1,563 research outputs found
The NextGen Model Atmosphere grid: II. Spherically symmetric model atmospheres for giant stars with effective temperatures between 3000 and 6800~K
We present the extension of our NextGen model atmosphere grid to the regime
of giant stars. The input physics of the models presented here is nearly
identical to the NextGen dwarf atmosphere models, however spherical geometry is
used self-consistently in the model calculations (including the radiative
transfer). We re-visit the discussion of the effects of spherical geometry on
the structure of the atmospheres and the emitted spectra and discuss the
results of NLTE calculations for a few selected models.Comment: ApJ, in press (November 1999), 13 pages, also available at
http://dilbert.physast.uga.edu/~yeti/PAPERS and at
ftp://calvin.physast.uga.edu/pub/preprints/NG-giants.ps.g
Stellar Population Models and Individual Element Abundances I: Sensitivity of Stellar Evolution Models
Integrated light from distant galaxies is often compared to stellar
population models via the equivalent widths of spectral features--spectral
indices--whose strengths rely on the abundances of one or more elements. Such
comparisons hinge not only on the overall metal abundance but also on relative
abundances. Studies have examined the influence of individual elements on
synthetic spectra but little has been done to address similar issues in the
stellar evolution models that underlie most stellar population models. Stellar
evolution models will primarily be influenced by changes in opacities. In order
to explore this issue in detail, twelve sets of stellar evolution tracks and
isochrones have been created at constant heavy element mass fraction Z that
self-consistently account for varying heavy element mixtures. These sets
include scaled-solar, alpha-enhanced, and individual cases where the elements
C, N, O, Ne, Mg, Si, S, Ca, Ti, and Fe have been enhanced above their
scaled-solar values. The variations that arise between scaled-solar and the
other cases are examined with respect to the H-R diagram and main sequence
lifetimes.Comment: 33 pages, 13 figures, accepted to Ap
The Red Rectangle: Its Shaping Mechanism and its Source of Ultraviolet Photons
The proto-planetary Red Rectangle nebula is powered by HD 44179, a
spectroscopic binary (P = 318 d), in which a luminous post-AGB component is the
primary source of both luminosity and current mass loss. Here, we present the
results of a seven-year, eight-orbit spectroscopic monitoring program of HD
44179, designed to uncover new information about the source of the
Lyman/far-ultraviolet continuum in the system as well as the driving mechanism
for the bipolar outflow producing the current nebula. Our observations of the
H-alpha line profile around the orbital phase of superior conjunction reveal
the secondary component to be the origin of the fast (max. v~560^{-1}\sun_{max} \ge 17,0002 -
5\times10^{-5}\sun^{-1}\sun$, about 5% of the
luminosity of the entire system. (abridged)Comment: Accepted for publication in Ap
Emergence of Classical BSE Strain Properties during Serial Passages of H-BSE in Wild-Type Mice
BACKGROUND: Two distinct forms of atypical spongiform encephalopathies (H-BSE and L-BSE) have recently been identified in cattle. Transmission studies in several wild-type or transgenic mouse models showed that these forms were associated with two distinct major strains of infectious agents, which also differed from the unique strain that had been isolated from cases of classical BSE during the food-borne epizootic disease. METHODOLOGY/PRINCIPAL FINDINGS: H-BSE was monitored during three serial passages in C57BL/6 mice. On second passage, most of the inoculated mice showed molecular features of the abnormal prion protein (PrP(d)) and brain lesions similar to those observed at first passage, but clearly distinct from those of classical BSE in this mouse model. These features were similarly maintained during a third passage. However, on second passage, some of the mice exhibited distinctly different molecular and lesion characteristics, reminiscent of classical BSE in C57Bl/6 mice. These similarities were confirmed on third passage from such mice, for which the same survival time was also observed as with classical BSE adapted to C57Bl/6 mice. Lymphotropism was rarely detected in mice with H-BSE features. In contrast, PrP(d) was detectable, on third passage, in the spleens of most mice exhibiting classical BSE features, the pattern being indistinguishable from that found in C57Bl/6 mice infected with classical BSE. CONCLUSION/SIGNIFICANCE: Our data demonstrate the emergence of a prion strain with features similar to classical BSE during serial passages of H-BSE in wild-type mice. Such findings might help to explain the origin of the classical BSE epizootic disease, which could have originated from a putatively sporadic form of BSE
Prion Seeding Activities of Mouse Scrapie Strains with Divergent PrPSc Protease Sensitivities and Amyloid Plaque Content Using RT-QuIC and eQuIC
Rona Barron - ORCID: 0000-0003-4512-9177
https://orcid.org/0000-0003-4512-9177Different transmissible spongiform encephalopathy (TSE)-associated forms of prion protein (e.g. PrPSc) can vary markedly in ultrastructure and biochemical characteristics, but each is propagated in the host. PrPSc propagation involves conversion from its normal isoform, PrPC, by a seeded or templated polymerization mechanism. Such a mechanism is also the basis of the RT-QuIC and eQuIC prion assays which use recombinant PrP (rPrPSen) as a substrate. These ultrasensitive detection assays have been developed for TSE prions of several host species and sample tissues, but not for murine models which are central to TSE pathogenesis research. Here we have adapted RT-QuIC and eQuIC to various murine prions and evaluated how seeding activity depends on glycophosphatidylinositol (GPI) anchoring and the abundance of amyloid plaques and protease-resistant PrPSc (PrPRes). Scrapie brain dilutions up to 10−8 and 10−13 were detected by RT-QuIC and eQuIC, respectively. Comparisons of scrapie-affected wild-type mice and transgenic mice expressing GPI anchorless PrP showed that, although similar concentrations of seeding activity accumulated in brain, the heavily amyloid-laden anchorless mouse tissue seeded more rapid reactions. Next we compared seeding activities in the brains of mice with similar infectivity titers, but widely divergent PrPRes levels. For this purpose we compared the 263K and 139A scrapie strains in transgenic mice expressing P101L PrPC. Although the brains of 263K-affected mice had little immunoblot-detectable PrPRes, RT-QuIC indicated that seeding activity was comparable to that associated with a high-PrPRes strain, 139A. Thus, in this comparison, RT-QuIC seeding activity correlated more closely with infectivity than with PrPRes levels. We also found that eQuIC, which incorporates a PrPSc immunoprecipitation step, detected seeding activity in plasma from wild-type and anchorless PrP transgenic mice inoculated with 22L, 79A and/or RML scrapie strains. Overall, we conclude that these new mouse-adapted prion seeding assays detect diverse types of PrPSc.https://doi.org/10.1371/journal.pone.00489697pubpub1
STELLAR POPULATION MODELS AND INDIVIDUAL ELEMENT ABUNDANCES. II. STELLAR SPECTRA AND INTEGRATED LIGHT MODELS
ABSTRACT The first paper in this series explored the effects of altering the chemical mixture of the stellar population on an element-by-element basis on stellar evolutionary tracks and isochrones to the end of the red giant branch. This paper extends the discussion by incorporating the fully consistent synthetic stellar spectra with those isochrone models in predicting integrated colors, Lick indices, and synthetic spectra. Older populations display element ratio effects in their spectra at higher amplitude than younger populations. In addition, spectral effects in the photospheres of stars tend to dominate over effects from isochrone temperatures and lifetimes, but, further, the isochrone-based effects that are present tend to fall along the age-metallicity degeneracy vector, while the direct stellar spectral effects usually show considerable orthogonality
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Circulating Mitochondrial DNA in Patients in the ICU as a Marker of Mortality: Derivation and Validation
Background: Mitochondrial DNA (mtDNA) is a critical activator of inflammation and the innate immune system. However, mtDNA level has not been tested for its role as a biomarker in the intensive care unit (ICU). We hypothesized that circulating cell-free mtDNA levels would be associated with mortality and improve risk prediction in ICU patients. Methods and Findings: Analyses of mtDNA levels were performed on blood samples obtained from two prospective observational cohort studies of ICU patients (the Brigham and Women's Hospital Registry of Critical Illness [BWH RoCI, n = 200] and Molecular Epidemiology of Acute Respiratory Distress Syndrome [ME ARDS, n = 243]). mtDNA levels in plasma were assessed by measuring the copy number of the NADH dehydrogenase 1 gene using quantitative real-time PCR. Medical ICU patients with an elevated mtDNA level (≥3,200 copies/µl plasma) had increased odds of dying within 28 d of ICU admission in both the BWH RoCI (odds ratio [OR] 7.5, 95% CI 3.6–15.8, p = 1×10−7) and ME ARDS (OR 8.4, 95% CI 2.9–24.2, p = 9×10−5) cohorts, while no evidence for association was noted in non-medical ICU patients. The addition of an elevated mtDNA level improved the net reclassification index (NRI) of 28-d mortality among medical ICU patients when added to clinical models in both the BWH RoCI (NRI 79%, standard error 14%, p<1×10−4) and ME ARDS (NRI 55%, standard error 20%, p = 0.007) cohorts. In the BWH RoCI cohort, those with an elevated mtDNA level had an increased risk of death, even in analyses limited to patients with sepsis or acute respiratory distress syndrome. Study limitations include the lack of data elucidating the concise pathological roles of mtDNA in the patients, and the limited numbers of measurements for some of biomarkers. Conclusions: Increased mtDNA levels are associated with ICU mortality, and inclusion of mtDNA level improves risk prediction in medical ICU patients. Our data suggest that mtDNA could serve as a viable plasma biomarker in medical ICU patients. Please see later in the article for the Editors' Summar
Serum proteomic analysis identifies sex-specific differences in lipid metabolism and inflammation profiles in adults diagnosed with Asperger syndrome
Background: The higher prevalence of Asperger Syndrome (AS) and other autism spectrum conditions in males has been known for many years. However, recent multiplex immunoassay profiling studies have shown that males and females with AS have distinct proteomic changes in serum. Methods. Here, we analysed sera from adults diagnosed with AS (males = 14, females = 16) and controls (males = 13, females = 16) not on medication at the time of sample collection, using a combination of multiplex immunoassay and shotgun label-free liquid chromatography mass spectrometry (LC-MS§ssup§E§esup§). The main objective was to identify sex-specific serum protein changes associated with AS. Results: Multiplex immunoassay profiling led to identification of 16 proteins that were significantly altered in AS individuals in a sex-specific manner. Three of these proteins were altered in females (ADIPO, IgA, APOA1), seven were changed in males (BMP6, CTGF, ICAM1, IL-12p70, IL-16, TF, TNF-alpha) and six were changed in both sexes but in opposite directions (CHGA, EPO, IL-3, TENA, PAP, SHBG). Shotgun LC-MS§ssup§E§esup§ profiling led to identification of 13 serum proteins which had significant sex-specific changes in the AS group and, of these, 12 were altered in females (APOC2, APOE, ARMC3, CLC4K, FETUB, GLCE, MRRP1, PTPA, RN149, TLE1, TRIPB, ZC3HE) and one protein was altered in males (RGPD4). The free androgen index in females with AS showed an increased ratio of 1.63 compared to controls. Conclusion: Taken together, the serum multiplex immunoassay and shotgun LC- MS§ssup§E§esup§ profiling results indicate that adult females with AS had alterations in proteins involved mostly in lipid transport and metabolism pathways, while adult males with AS showed changes predominantly in inflammation signalling. These results provide further evidence that the search for biomarkers or novel drug targets in AS may require stratification into male and female subgroups, and could lead to the development of novel targeted treatment approaches
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