1,865 research outputs found
A unified first-principles study of Gilbert damping, spin-flip diffusion and resistivity in transition metal alloys
Using a formulation of first-principles scattering theory that includes
disorder and spin-orbit coupling on an equal footing, we calculate the
resistivity , spin flip diffusion length and the Gilbert damping
parameter for NiFe substitutional alloys as a function of
. For the technologically important NiFe alloy, permalloy, we
calculate values of Ohm-cm, nm,
and compared to experimental low-temperature values
in the range Ohm-cm for , nm for , and
for indicating that the theoretical formalism captures
the most important contributions to these parameters.Comment: Published in Physical Review Letter
Association between infectious burden, socioeconomic status, and ischemic stroke
Background and aims: Infectious diseases contribute to stroke risk, and are associated with socioeconomic status (SES). We tested the hypotheses that the aggregate burden of infections increases the risk of ischemic stroke (IS) and partly explains the association between low SES and ischemic stroke. Methods: In a case-control study with 470 ischemic stroke patients and 809 age- and sex-matched controls, randomly selected from the population, antibodies against the periodontal microbial agents Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, against Chlamydia pneumonia, Mycoplasma pneumoniae (IgA and IgG), and CagA-positive Helicobacter pylori (IgG) were assessed. Results: IgA seropositivity to two microbial agents was significantly associated with IS after adjustment for SES (OR 1.45 95% CI 1.01-2.08), but not in the fully adjusted model (OR 1.32 95% CI 0.86-2.02). By trend, cumulative IgA seropositivity was associated with stroke due to large vessel disease (LVD) after full adjustment (OR 1.88, 95% CI 0.96e3.69). Disadvantageous childhood SES was associated with higher cumulative seropositivity in univariable analyses, however, its strong impact on stroke risk was not influenced by seroepidemiological data in the multivariable model. The strong association between adulthood SES and stroke was rendered nonsignificant when factors of dental care were adjusted for. Conclusions: Infectious burden assessed with five microbial agents did not independently contribute to ischemic stroke consistently, but may contribute to stroke due to LVD. High infectious burden may not explain the association between childhood SES and stroke risk. Lifestyle factors that include dental negligence may contribute to the association between disadvantageous adulthood SES and stroke. (C) 2016 Elsevier Ireland Ltd. All rights reserved.Peer reviewe
A shared compilation stack for distributed-memory parallelism in stencil DSLs
Domain Specific Languages (DSLs) increase programmer productivity and provide
high performance. Their targeted abstractions allow scientists to express
problems at a high level, providing rich details that optimizing compilers can
exploit to target current- and next-generation supercomputers. The convenience
and performance of DSLs come with significant development and maintenance
costs. The siloed design of DSL compilers and the resulting inability to
benefit from shared infrastructure cause uncertainties around longevity and the
adoption of DSLs at scale. By tailoring the broadly-adopted MLIR compiler
framework to HPC, we bring the same synergies that the machine learning
community already exploits across their DSLs (e.g. Tensorflow, PyTorch) to the
finite-difference stencil HPC community. We introduce new HPC-specific
abstractions for message passing targeting distributed stencil computations. We
demonstrate the sharing of common components across three distinct HPC
stencil-DSL compilers: Devito, PSyclone, and the Open Earth Compiler, showing
that our framework generates high-performance executables based upon a shared
compiler ecosystem
Matrix Metalloproteinase-Mediated Blood-Brain Barrier Dysfunction in Epilepsy
The blood-brain barrier is dysfunctional in epilepsy, thereby contributing to seizure genesis and resistance to antiseizure drugs. Previously, several groups reported that seizures increase brain glutamate levels, which leads to barrier dysfunction. One critical component of barrier dysfunction is brain capillary leakage. Based on our preliminary data, we hypothesized that glutamate released during seizures mediates an increase in matrix-metalloproteinase (MMP) expression and activity levels, thereby contributing to barrier leakage. To test this hypothesis, we exposed isolated brain capillaries from male Sprague Dawley rats to glutamate ex vivo and used an in vivo/ex vivo approach of isolated brain capillaries from female Wistar rats that experienced status epilepticus as an acute seizure model. We found that exposing isolated rat brain capillaries to glutamate increased MMP-2 and MMP-9 protein and activity levels, and decreased tight junction protein levels, which resulted in barrier leakage. We confirmed these findings in vivo in rats after status epilepticus and in brain capillaries from male mice lacking cytosolic phospholipase A2. Together, our data support the hypothesis that glutamate released during seizures signals an increase in MMP-2 and MMP-9 protein expression and activity levels, resulting in blood-brain barrier leakage
Characterization of grain boundaries in multicrystalline silicon with high lateral resolution using conductive atomic force microscopy
In this work, the electrical characteristics of grain boundaries (GBs) in multicrystalline silicon with and without iron contamination are analyzed by fixed voltage current maps and local I/V curves using conductive AFM (cAFM). I/V characteristics reveal the formation of a Schottky contact between the AFM tip and the sample surface. The impact of both, the polarity of the applied voltage and the illumination by the AFM laser on the behavior of GBs was analyzed systematically. Depending on the polarity of the applied voltage and the iron content of the sample, grain boundaries alter significantly the recorded current flow compared to the surrounding material. The results also show a clear influence of the AFM laser light on the electrical behavior of the grain boundaries. Conductive AFM measurements are furthermore compared to data obtained by electron beam induced current (EBIC), indicating that cAFM provides complimentary information
The Nature of Optically Dull Active Galactic Nuclei in COSMOS
We present infrared, optical, and X-ray data of 48 X-ray bright, optically
dull AGNs in the COSMOS field. These objects exhibit the X-ray luminosity of an
active galactic nucleus (AGN) but lack broad and narrow emission lines in their
optical spectrum. We show that despite the lack of optical emission lines, most
of these optically dull AGNs are not well-described by a typical passive red
galaxy spectrum: instead they exhibit weak but significant blue emission like
an unobscured AGN. Photometric observations over several years additionally
show significant variability in the blue emission of four optically dull AGNs.
The nature of the blue and infrared emission suggest that the optically
inactive appearance of these AGNs cannot be caused by obscuration intrinsic to
the AGNs. Instead, up to ~70% of optically dull AGNs are diluted by their
hosts, with bright or simply edge-on hosts lying preferentially within the
spectroscopic aperture. The remaining ~30% of optically dull AGNs have
anomalously high f_x/f_o ratios and are intrinsically weak, not obscured, in
the optical. These optically dull AGNs are best described as a weakly accreting
AGN with a truncated accretion disk from a radiatively inefficient accretion
flow.Comment: 12 pages, 10 figures. Accepted for publication in the Ap
Matched sizes of activating and inhibitory receptor/ligand pairs are required for optimal signal integration by human Natural Killer cells
It has been suggested that receptor-ligand complexes segregate or co-localise within immune synapses according to their size, and this is important for receptor signaling. Here, we set out to test the importance of receptor-ligand complex dimensions for immune surveillance of target cells by human Natural Killer (NK) cells. NK cell activation is regulated by integrating signals from activating receptors, such as NKG2D, and inhibitory receptors, such as KIR2DL1. Elongating the NKG2D ligand MICA reduced its ability to trigger NK cell activation. Conversely, elongation of KIR2DL1 ligand HLA-C reduced its ability to inhibit NK cells. Whereas normal-sized HLA-C was most effective at inhibiting activation by normal-length MICA, only elongated HLA-C could inhibit activation by elongated MICA. Moreover, HLA-C and MICA that were matched in size co-localised, whereas HLA-C and MICA that were different in size were segregated. These results demonstrate that receptor-ligand dimensions are important in NK cell recognition, and suggest that optimal integration of activating and inhibitory receptor signals requires the receptor-ligand complexes to have similar dimensions
AEGIS: Demographics of X-ray and Optically Selected AGNs
We develop a new diagnostic method to classify galaxies into AGN hosts,
star-forming galaxies, and absorption-dominated galaxies by combining the [O
III]/Hbeta ratio with rest-frame U-B color. This can be used to robustly select
AGNs in galaxy samples at intermediate redshifts (z<1). We compare the result
of this optical AGN selection with X-ray selection using a sample of 3150
galaxies with 0.3<z<0.8 and I_AB<22, selected from the DEEP2 Galaxy Redshift
Survey and the All-wavelength Extended Groth Strip International Survey
(AEGIS). Among the 146 X-ray sources in this sample, 58% are classified
optically as emission-line AGNs, the rest as star-forming galaxies or
absorption-dominated galaxies. The latter are also known as "X-ray bright,
optically normal galaxies" (XBONGs). Analysis of the relationship between
optical emission lines and X-ray properties shows that the completeness of
optical AGN selection suffers from dependence on the star formation rate and
the quality of observed spectra. It also shows that XBONGs do not appear to be
a physically distinct population from other X-ray detected, emission-line AGNs.
On the other hand, X-ray AGN selection also has strong bias. About 2/3 of all
emission-line AGNs at L_bol>10^44 erg/s in our sample are not detected in our
200 ks Chandra images, most likely due to moderate or heavy absorption by gas
near the AGN. The 2--7 keV detection rate of Seyfert 2s at z~0.6 suggests that
their column density distribution and Compton-thick fraction are similar to
that of local Seyferts. Multiple sample selection techniques are needed to
obtain as complete a sample as possible.Comment: 24 pages, 14 figures, submitted to ApJ. Version 2 matches the ApJ
accepted version. Sec 3 was reorganized and partly rewritten with one
additional figure (Fig.3
SHARPIN Negatively Associates with TRAF2-Mediated NFκB Activation
NFκB is an inducible transcriptional factor controlled by two principal signaling cascades and plays pivotal roles in diverse physiological processes including inflammation, apoptosis, oncogenesis, immunity, and development. Activation of NFκB signaling was detected in skin of SHAPRIN-deficient mice and can be diminished by an NFκB inhibitor. However, in vitro studies demonstrated that SHARPIN activates NFκB signaling by forming a linear ubiquitin chain assembly complex with RNF31 (HOIP) and RBCK1 (HOIL1). The inconsistency between in vivo and in vitro findings about SHARPIN's function on NFκB activation could be partially due to SHARPIN's potential interactions with downstream molecules of NFκB pathway. In this study, 17 anti-flag immunoprecipitated proteins, including TRAF2, were identified by mass spectrum analysis among Sharpin-Flag transfected mouse fibroblasts, B lymphocytes, and BALB/c LN stroma 12 cells suggesting their interaction with SHARPIN. Interaction between SHARPIN and TRAF2 confirmed previous yeast two hybridization reports that SHARPIN was one TRAF2's partners. Furthermore, luciferase-based NFκB reporter assays demonstrated that SHARPIN negatively associates with NFκB activation, which can be partly compensated by over-expression of TRAF2. These data suggested that other than activating NFκB signaling by forming ubiquitin ligase complex with RNF31 and RBCK1, SHARPIN may also negatively associate with NFκB activation via interactions with other NFκB members, such as TRAF2
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