141 research outputs found
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X-Ray Scattering Studies of the SiO/Si(001) Interfacial Structure
X‐ray scattering has been utilized in a study of the SiO/Si(001) interfacial structure. Scattering data provide evidence for a low coverage 2×1 epitaxial structure at the SiO/Si interface for dry oxides grown on highly ordered Si surfaces at room temperature. The observed scattering is consistent with distorted dimer models of the interfacial structure. Thermal annealing substantially reduces the order of the 2×1 structure while prolonged exposure to humid air almost eliminates the 2×1 symmetry scattering. These findings suggest that the observed 2×1 order is associated with a metastable, intermediate state of the dry oxidation process.Engineering and Applied Science
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X‐Ray Reflectivity Studies of SiO/Si(001)
X‐ray reflectivity has been utilized in a study of the SiO/Si interfacial structure for dry oxides grown at room temperature on highly ordered Si(001) surfaces. Scattering near (110) demonstrates the Si lattice termination of the wafers studied is characterized by a highly ordered array of terraces separated by monoatomic steps. Specular reflectivity data indicate the ‘‘native’’ dry oxide thickness is approximately 5 Å with a 1‐Å vacuum interface width. Residual laminar order in the oxide electron density along the oxide/Si interfacial normal decays exponentially from the oxide/Si interface with a 2.7‐Å decay length.Engineering and Applied Science
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X-Ray Grazing Incidence Diffraction from Alkylsiloxane Monolayers on Silicon Wafers
X‐ray reflection (both specular and off‐specular) and grazing incidence diffraction (GID) have been used to study the structure of alkylsiloxane monolayers () formed by self‐assembly from solution on silicon wafers. GID studies of complete monolayers reveal a single ring of scattering associated with the monolayer. The Lorentzian line shape of this ring indicates that the film is characterized by liquidlike order, with a typical translational correlation length of about 45 Å. The thermal coefficient of expansion of the monolayer, as determined from the GID peak position, is approximately equal to the value for liquid n‐alkanes. Upon either heating or cooling, the monolayer correlation lengths decrease, suggesting that the differential thermal‐expansion coefficients of the film and substrate figure prominently in thermal changes of the molecular ordering. GID data for incomplete monolayers also reveal a single ring of scattering associated with the monolayer. While both the translational correlation lengths and integrated peak areas are significantly reduced relative to complete monolayers, the peak positions of the incomplete monolayers are comparable to those of complete monolayers. Given the lower average areal density of incomplete monolayers, this finding implies that incomplete monolayers are inhomogeneous.Engineering and Applied Science
A direct D-bar reconstruction algorithm for recovering a complex conductivity in 2-D
A direct reconstruction algorithm for complex conductivities in
, where is a bounded, simply connected Lipschitz
domain in , is presented. The framework is based on the
uniqueness proof by Francini [Inverse Problems 20 2000], but equations relating
the Dirichlet-to-Neumann to the scattering transform and the exponentially
growing solutions are not present in that work, and are derived here. The
algorithm constitutes the first D-bar method for the reconstruction of
conductivities and permittivities in two dimensions. Reconstructions of
numerically simulated chest phantoms with discontinuities at the organ
boundaries are included.Comment: This is an author-created, un-copyedited version of an article
accepted for publication in [insert name of journal]. IOP Publishing Ltd is
not responsible for any errors or omissions in this version of the manuscript
or any version derived from it. The Version of Record is available online at
10.1088/0266-5611/28/9/09500
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X-Ray Specular Reflection Studies of Silicon Coated by Organic Monolayers (Alkylsiloxanes)
X-ray specular reflectivity has been used to characterize the structure of silicon–silicon-oxide surfaces coated with chemisorbed hydrocarbon monolayer films (alkylsiloxanes). Using synchrotron radiation the reflectivity was followed over 9 orders of magnitude, from grazing incidence to an incident angle of φ≊6.5°, or q=(4π/λ)sin(φ)=0.8 Å-1, allowing a spatial resolution of features approximately π/0.8≊4.0 Å along the surface normal. Analysis was performed by fitting the data to reflectivities calculated from models of the surface electron density and by calculating Patterson functions directly from the data. Although the measured reflectivities could be equally well described by different sets of model parameters, the electron densities calculated from these different parameters were remarkably alike. Inspection of the electron densities allowed identification of a layer of SiO2 (≊17-Å thick), a layer of head-group region where the alkylsiloxane adsorbs to the SiO2, and the hydrocarbon layer. Fitting the data also required that the various interfaces have different widths. The fact that the same local hydrocarbon density of 0.85 g/cm3 was observed for both fully formed and partially formed monolayers with alkane chains of varying length excluded a model in which the partially formed monolayer was made up of separated islands of well-formed monolayers. Measurements before and after chemical reaction of a monolayer in which the alkyl chain was terminated by an olefinic group demonstrated the ability to use x-ray reflectivity to characterize chemical changes. The effects of radiation damage on these types of measurements are described.Engineering and Applied Science
The V471A polymorphism in autophagy-related gene ATG7 modifies age at onset specifically in Italian Huntington disease patients
The cause of Huntington disease (HD) is a polyglutamine repeat expansion of more than 36 units in the huntingtin protein, which is inversely correlated with the age at onset of the disease. However, additional genetic factors are believed to modify the course and the age at onset of HD. Recently, we identified the V471A polymorphism in the autophagy-related gene ATG7, a key component of the autophagy pathway that plays an important role in HD pathogenesis, to be associated with the age at onset in a large group of European Huntington disease patients. To confirm this association in a second independent patient cohort, we analysed the ATG7 V471A polymorphism in additional 1,464 European HD patients of the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). In the entire REGISTRY cohort we could not confirm a modifying effect of the ATG7 V471A polymorphism. However, analysing a modifying effect of ATG7 in these REGISTRY patients and in patients of our previous HD cohort according to their ethnic origin, we identified a significant effect of the ATG7 V471A polymorphism on the HD age at onset only in the Italian population (327 patients). In these Italian patients, the polymorphism is associated with a 6-years earlier disease onset and thus seems to have an aggravating effect. We could specify the role of ATG7 as a genetic modifier for HD particularly in the Italian population. This result affirms the modifying influence of the autophagic pathway on the course of HD, but also suggests population-specific modifying mechanisms in HD pathogenesis
Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study
Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation
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