Copper deposition on TiO2 from copper(II)hexafluoroacetylacetonate

The authors have studied the adsorption of CuII(hfac)2 on the surface of a model oxide system, TiO2(110), and probed the molecular stability with respect to thermal cycling, using atomic scale imaging by scanning tunneling microscopy supported by x-ray photoemission spectroscopy. They find that at 473 K, the adsorbed metal-organic molecules begin to dissociate and release Cu atoms which aggregate and form Cu nanoparticles. These Cu nanoparticles ripen over time and the size (height) distribution develops into a bimodal distribution. Unlike other organometallic systems, which show a bimodal distribution due to enhanced nucleation or growth at surface step edges, the nanoparticles do not preferentially form at steps. The reduced mobility of the Cu islands may be related to the co-adsorbed ligands that remain in very small clusters on the surface

Chromium nanostructures formed by dewetting of heteroepitaxial films on W(100)

In this paper, we report the surprising formation of square-based facetted islands with linear dimension of the order of 500 nm upon dewetting of a Cr multilayer onW(100).We show that these square islands are composed of inclined facets surrounding a depressed center such that the facet slopes inward with the outer edges of the islands thicker than the centers. The islands’ shapes do not represent traditional equilibrium crystal shapes as expected for a Wulf construction. In situ UV and x-ray photoelectron emission microscopy allied to spatially resolved spectroscopy throws considerable light on the nature of the dewetting and shows that the metal surface between the islands remains covered by a thin pseudomorphic wetting layer of ∼1 ML. Low-energy electron diffraction and scanning tunneling and atomic force microscopies allow quantification of facet slopes, and we identify a predominance of tilted Cr(100) facets ±5◦ off of the substrate normal bound by (210) planes at ∼26◦. The epitaxial Cr islands adopt the bulk Cr lattice constant but are tilted with respect to the surface normal.We suggest that the Cr crystallite tilting creates a vicinal-like interface structure that determines the island morpholog

The GABBR1 locus and the G1465A variant is not associated with temporal lobe epilepsy preceded by febrile seizures

BACKGROUND: Polymorphism G1465A in the GABBR1 gene has been suggested as a risk factor for non-lesional temporal lobe epilepsy (TLE); however, this genetic association study has not been independently replicated. We attempted to replicate this study in our cohort of patients with TLE. Furthermore, we also analyzed the coding sequence of this gene and searched for disease-causing mutations. METHODS: We included 120 unrelated individuals with TLE that was preceded by febrile seizures (FS) who did not have any evidence of structural lesions suggesting secondary epilepsy. 66 individuals had positive family history of TLE epilepsy and 54 were sporadic. Each patient was genotyped for the presence of G1465A polymorphism. All exons of the GABBR1 gene were screened by single strand confirmation polymorphism method. Genotypes were compared with two independent matched control groups. RESULTS: We detected two A alleles of the G1465A polymorphism in one homozygous control subject (0.87% of all alleles) and one A allele in a patient with TLE (0.45%, not significant). Other detected polymorphisms in coding regions had similar frequencies in epilepsy patients and control groups. No disease causing mutations in the GABBR1 gene were detected in patients with sporadic or familial TLE. CONCLUSION: Our results indicate that TLE preceded by FS is not associated with the polymorphisms or mutations in the GABBR1 gene, including the G1465A polymorphism. The proportion of TLE patients with FS in the original study, reporting this positive association, did not differ between allele A negative and positive cases. Thus, our failure to reproduce this result is likely applicable to all non-lesional TLE epilepsies

Charge transfer in Cr adsorption and reaction at the rutile TiO2(110) surface

The rutile TiO2(110) surface has been doped with sub-monolayer metallic Cr, which oxidises and donates charge to specific surface Ti ions. X-Ray and ultra violet photoemission spectroscopy and first principles density functional theory with Hubbard U are used to assign the oxidation states of Cr and surface Ti and we find that Cr2+ forms on bridging oxygen ions and a 5-fold coordinated surface Ti atom is reduced to Ti3+ and the Cr ions readily react with oxygen (to Cr3+), which leads to depletion of surface Ti3+ 3d electrons

De-novo mutations of the sodium channel gene SCN1A in alleged vaccine encephalopathy: a retrospective study

Copyright © 2006 Elsevier Ltd All rights reserved.BackgroundVaccination, particularly for pertussis, has been implicated as a direct cause of an encephalopathy with refractory seizures and intellectual impairment. We postulated that cases of so-called vaccine encephalopathy could have mutations in the neuronal sodium channel alpha1 subunit gene (SCN1A) because of a clinical resemblance to severe myoclonic epilepsy of infancy (SMEI) for which such mutations have been identified.MethodsWe retrospectively studied 14 patients with alleged vaccine encephalopathy in whom the first seizure occurred within 72 h of vaccination. We reviewed the relation to vaccination from source records and assessed the specific epilepsy phenotype. Mutations in SCN1A were identified by PCR amplification and denaturing high performance liquid chromatography analysis, with subsequent sequencing. Parental DNA was examined to ascertain the origin of the mutation.FindingsSCN1A mutations were identified in 11 of 14 patients with alleged vaccine encephalopathy; a diagnosis of a specific epilepsy syndrome was made in all 14 cases. Five mutations predicted truncation of the protein and six were missense in conserved regions of the molecule. In all nine cases where parental DNA was available the mutations arose de novo. Clinical-molecular correlation showed mutations in eight of eight cases with phenotypes of SMEI, in three of four cases with borderline SMEI, but not in two cases with Lennox-Gastaut syndrome.InterpretationCases of alleged vaccine encephalopathy could in fact be a genetically determined epileptic encephalopathy that arose de novo. These findings have important clinical implications for diagnosis and management of encephalopathy and, if confirmed in other cohorts, major societal implications for the general acceptance of vaccination.Samuel F Berkovic, Louise Harkin, Jacinta M McMahon, James T Pelekanos, Sameer M Zuberi, Elaine C Wirrell, Deepak S Gill, Xenia Iona, John C Mulley and Ingrid E Schefferhttp://www.elsevier.com/wps/find/journaldescription.cws_home/622235/description#descriptio

9th International workshop on Fragile X syndrome and X-linked mental retardation

No abstract availabl

Mutations in DEPDC5 cause familial focal epilepsy with variable foci

<p>The majority of epilepsies are focal in origin, with seizures emanating from one brain region. Although focal epilepsies often arise from structural brain lesions, many affected individuals have normal brain imaging. The etiology is unknown in the majority of individuals, although genetic factors are increasingly recognized. Autosomal dominant familial focal epilepsy with variable foci (FFEVF) is notable because family members have seizures originating from different cortical regions(1). Using exome sequencing, we detected DEPDC5 mutations in two affected families. We subsequently identified mutations in five of six additional published large families with FFEVF. Study of families with focal epilepsy that were too small for conventional clinical diagnosis with FFEVF identified DEPDC5 mutations in approximately 12% of families (10/82). This high frequency establishes DEPDC5 mutations as a common cause of familial focal epilepsies. Shared homology with G protein signaling molecules and localization in human neurons suggest a role of DEPDC5 in neuronal signal transduction.</p>