Here, we present a new code, CASTRO, that solves the multicomponent compressible hydrodynamic equations for astrophysical flows including self-gravity, nuclear reactions, and radiation. CASTRO uses ...an Eulerian grid and incorporates adaptive mesh refinement (AMR). Our approach to AMR uses a nested hierarchy of logically rectangular grids with simultaneous refinement in both space and time. The radiation component of CASTRO will be described in detail in the next paper, Part II, of this series.
We present the first three-dimensional, full-star simulations of convection in a white dwarf preceding a Type Ia supernova, specifically the last few hours before ignition. For these long-time ...calculations, we use our low Mach number hydrodynamics code, MAESTRO, which we have further developed to treat spherical stars centered in a three-dimensional Cartesian geometry. The main change required is a procedure to map the one-dimensional radial base state to and from the Cartesian grid. Our models recover the dipole structure of the flow seen in previous calculations, but our long-time integration shows that the orientation of the dipole changes with time. Furthermore, we show the development of gravity waves in the outer, stable portion of the star. Finally, we evolve several calculations to the point of ignition and discuss the range of ignition radii.
2,3,7,8-Tetrachlorodibenzo-
p-dioxin (TCDD) is highly toxic in experimental animals, and is known to induce cytochrome P450 (
CYP) gene expression. We investigated the effect of
CYP1A1 and
CYP1B1 ...variant genotypes and haplotypes on
CYP1A1 and
CYP1B1 mRNA expression and ethoxyresorufin-
O-deethylase (EROD) activity in lymphocytes from 121 subjects from the Seveso population, Italy, accidentally exposed to TCDD in 1976. The 3′UTR 3801T>C and I462V variants of
CYP1A1 were present in 16% and 6% of the subjects, respectively. The frequency of
CYP1B1 variants was 85.2% for L432V, 49.6% for R48G and A119S, and 28.7% for N453S. There was complete linkage disequilibrium (LD) among the
CYP1B1 variant loci (
D′
=
−1) and high LD among the
CYP1A1 loci (
D′
=
0.86). Gene expression measured by RT-PCR did not vary by
CYP1B1 genotype in uncultured lymphocytes. However, when lymphocytes were treated in vitro with 10
nM TCDD,
CYP1B1 and
CYP1A1 mRNA expression was strongly induced and modified by
CYP variant alleles. Specifically, the
CYP1B1*3 haplotype (L432V) was associated with increased
CYP1B1 mRNA expression (
P
=
0.03), following an additive model; the
CYP1A1 I462V polymorphism was positively, although not significantly, associated with
CYP1A1 expression. The
CYP1B1*3 variant may have affected
CYP1B1 expression in subjects highly and acutely exposed to dioxin at the time of the accident. Although based on small number of subjects, a slight increase in eczema (
P
=
0.05,
n
=
8) and urticaria (
P
=
0.02,
n
=
2) was observed 20 years after the accident in subjects carrying the
CYP1B1*3 allele. Genetic variation in cytochrome P450 induction may identify subjects with variable responsiveness to TCDD and potentially increased risk of disease.
The Amaldi 10 Parallel Session C3 on Advanced Gravitational Wave detectors gave an overview of the status and several specific challenges and solutions relevant to the instruments planned for a ...mid-decade start of observation. Invited overview talks for the Virgo, LIGO, and KAGRA instruments were complemented by more detailed discussions in presentations and posters of some instrument features and designs.
Neuromyelitis optica is an inflammatory demyelinating disease of the central nervous system associated with autoantibodies against the glial water channel protein aquaporin-4. It has recently been ...reported that immunoglobulin from neuromyelitis optica patients injected peripherally does not cause lesions in naive rats, but only when pre-existing central nervous system inflammation is present. Here, we investigated whether immunoglobulin G from aquaporin-4-autoantibody-positive neuromyelitis optica patients has the potential to damage the central nervous system either alone or in the presence of human complement. Immunoglobulin G from neuromyelitis optica patients did not activate mouse complement and was not pathogenic when injected into mouse brain. However, co-injection of immunoglobulin G from neuromyelitis optica patients with human complement produced neuromyelitis optica-like lesions in mice. Within 12 h of co-injecting immunoglobulin G from neuromyelitis optica patients and human complement, there was a striking loss of aquaporin-4 expression, glial cell oedema, myelin breakdown and axonal injury, but little intra-parenchymal inflammation. At 7 days, there was extensive inflammatory cell infiltration, perivascular deposition of activated complement components, extensive demyelination, loss of aquaporin-4 expression, loss of reactive astrocytes and neuronal cell death. In behavioural studies, mice injected with immunoglobulin G from neuromyelitis optica patients and human complement into the right hemisphere preferentially turned to the right at 7 days. No brain inflammation, demyelination or right-turning behaviour was seen in wild-type mice that received immunoglobulin G from non-neuromyelitis optica patients with human complement, or in aquaporin-4-null mice that received immunoglobulin G from neuromyelitis optica patients with human complement. We conclude that co-injection of immunoglobulin G from neuromyelitis optica patients with human complement reproduces the key histological features of neuromyelitis optica and that aquaporin-4 is necessary and sufficient for immunoglobulin G from neuromyelitis optica patients to exert its effect. In our mouse model, immunoglobulin G from neuromyelitis optica patients does not require pre-existing central nervous system inflammation to produce lesions.
The Spitzer Extended Deep Survey (SEDS) is a very deep infrared survey within five well-known extragalactic science fields: the UKIDSS Ultra-Deep Survey, the Extended Chandra Deep Field South, ...COSMOS, the Hubble Deep Field North, and the Extended Groth Strip. SEDS covers a total area of 1.46 deg super(2) to a depth of 26 AB mag (3sigma) in both of the warm Infrared Array Camera (IRAC) bands at 3.6 and 4.5 mum. Because of its uniform depth of coverage in so many widely-separated fields, SEDS is subject to roughly 25% smaller errors due to cosmic variance than a single-field survey of the same size. SEDS was designed to detect and characterize galaxies from intermediate to high redshifts (z = 2-7) with a built-in means of assessing the impact of cosmic variance on the individual fields. Because the full SEDS depth was accumulated in at least three separate visits to each field, typically with six-month intervals between visits, SEDS also furnishes an opportunity to assess the infrared variability of faint objects. This paper describes the SEDS survey design, processing, and publicly-available data products. Deep IRAC counts for the more than 300,000 galaxies detected by SEDS are consistent with models based on known galaxy populations. Discrete IRAC sources contribute 5.6 + or - 1.0 and 4.4 + or - 0.8 nW m super(-2) sr super(-1) at 3.6 and 4.5 mum to the diffuse cosmic infrared background (CIB). IRAC sources cannot contribute more than half of the total CIB flux estimated from DIRBE data. Barring an unexpected error in the DIRBE flux estimates, half the CIB flux must therefore come from a diffuse component.
ABSTRACT We present a catalog of visual-like H-band morphologies of ∼50.000 galaxies (Hf160w < 24.5) in the 5 CANDELS fields (GOODS-N, GOODS-S, UDS, EGS, and COSMOS). Morphologies are estimated using ...Convolutional Neural Networks (ConvNets). The median redshift of the sample is The algorithm is trained on GOODS-S, for which visual classifications are publicly available, and then applied to the other 4 fields. Following the CANDELS main morphology classification scheme, our model retrieves for each galaxy the probabilities of having a spheroid or a disk, presenting an irregularity, being compact or a point source, and being unclassifiable. ConvNets are able to predict the fractions of votes given to a galaxy image with zero bias and ∼10% scatter. The fraction of mis-classifications is less than 1%. Our classification scheme represents a major improvement with respect to Concentration-Asymmetry-Smoothness-based methods, which hit a 20%-30% contamination limit at high z. The catalog is released with the present paper via the Rainbow database (http://rainbowx.fis.ucm.es/Rainbow_navigator_public/).
Objective:
Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system associated with pathogenic autoantibodies against the astrocyte water channel protein ...aquaporin‐4 (AQP4). The presence of neutrophils is a characteristic feature in NMO lesions in humans. Neutrophils are not generally found in multiple sclerosis lesions. We evaluated the role of neutrophils in a mouse NMO model.
Methods:
NMO lesions were produced in mice by intracerebral injection of immunoglobulin G (IgG) isolated from NMO patient serum and human complement. We previously reported that this mouse model produces the characteristic histological features of NMO, including perivascular complement activation, inflammatory cell infiltration, and loss of myelin, AQP4, and glial fibrillary acidic protein. Lesions are absent when AQP4 null mice are used or when IgG from non‐NMO patients is injected.
Results:
We found remarkably reduced neuroinflammation, myelin loss, and AQP4 loss in brains of neutropenic mice at 24 hours and 7 days, and increased severity of NMO lesions in mice made neutrophilic by granulocyte colony stimulating factor. NMO lesions were greatly reduced by intracerebral administration of the neutrophil protease inhibitors Sivelestat and cathepsin G inhibitor I or by intraperitoneal injection of Sivelestat alone. Immunostaining of human NMO lesions for neutrophil elastase revealed many degranulating perivascular neutrophils, with no equivalent perivascular neutrophils in human multiple sclerosis lesions.
Interpretation:
Our data implicate a central role of neutrophils in the pathogenesis of early NMO lesions and suggest the potential utility of neutrophil protease inhibitors such as Sivelestat in NMO therapy. ANN NEUROL 2012;
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