475 research outputs found
The rapid evolution of the exciting star of the Stingray Nebula
SAO244567, the exciting star of the Stingray nebula, is rapidly evolving.
Previous analyses suggested that it has heated up from an effective temperature
of about 21kK in 1971 to over 50kK in the 1990s. Canonical post-asymptotic
giant branch evolution suggests a relatively high mass while previous analyses
indicate a low-mass star. Fitting line profiles from static and expanding
non-LTE model atmospheres to the observed UV and optical spectra, taken during
1988-2013, allowed us to study the temporal change of effective temperature,
surface gravity, mass-loss rate, and terminal wind velocity. In addition, we
determined the chemical composition of the atmosphere. We find that the central
star has steadily increased its effective temperature from 38kK in 1988 to a
peak value of 60kK in 2002. During the same time, the star was contracting, as
concluded from an increase in surface gravity from log g = 4.8 to 6.0 and a
drop in luminosity. Simultaneously, the mass-loss rate declined from log
(dM/dt/Msun/yr)=-9.0 to -11.6 and the terminal wind velocity increased from
1800km/s to 2800km/s. Since around 2002, the star stopped heating and has
cooled down again to 55kK by 2006. It has a largely solar surface composition
with the exception of slightly subsolar carbon, phosphorus, and sulfur. By
comparison with stellar-evolution calculations, we confirm that SAO244567 must
be a low-mass star (M < 0.55 Msun). However, the slow evolution of the
respective stellar evolutionary models is in strong contrast to the observed
fast evolution and the young planetary nebula with a kinematical age of only
about 1000 years. We speculate that the star could be a late He-shell flash
object. Alternatively, it could be the outcome of close-binary evolution. Then
SAO244567 would be a low-mass (0.354 Msun) helium prewhite dwarf after the
common-envelope phase, during which the planetary nebula was ejected.Comment: 16 pages, 13 figures, accepted for publication in A&
Sensors Best Paper Award 2015
Since 2011, an annual award system was instituted to recognize outstanding Sensors papers that are related to sensing technologies and applications and meet the aims, scope and high standards of this journal [1–4]. This year, the winners were chosen by the Section Editor-in-Chiefs of Sensors from among all the papers published in 2011 to track citations. Reviews and full research articles were considered separately. We gladly announce that the following eight papers were awarded the Sensors Best Paper Award in 2015
Perspectives on the Use of Multiple Sclerosis Risk Genes for Prediction
Objective: A recent collaborative genome-wide association study replicated a large number of susceptibility loci and identified novel loci. This increase in known multiple sclerosis (MS) risk genes raises questions about clinical applicability of genotyping. In an empirical set we assessed the predictive power of typing multiple genes. Next, in a modelling study we explored current and potential predictive performance of genetic MS risk models. Materials and Methods: Genotype data on 6 MS risk genes in 591 MS patients and 600 controls were used to investigate the predictive value of combining risk alleles. Next, the replicated and novel MS risk loci from the recent and largest international genome-wide association study were used to construct genetic risk models simulating a population of 100,000 individuals. Finally, we assessed the required numbers, frequencies, and ORs of risk SNPs for higher discriminative accuracy in the future. Results: Individuals with 10 to 12 risk alleles had a significantly increased risk compared to individuals with the average population risk for developing MS (OR 2.76 (95% CI 2.02-3.77)). In the simulation study we showed that the area under the receiver operating characteristic curve (AUC) for a risk score based on the 6 SNPs was 0.64. The AUC increases to 0.66 using the well replicated 24 SNPs and to 0.69 when including all replicated and novel SNPs (n = 53) in the risk model. An additional 20 SNPs with allele frequency 0.30 and ORs 1.1 would be needed to increase the AUC to a slightly higher level of 0.70, and at least 50 novel variants with allele frequency 0.30 and ORs 1.4 would be needed to obtain an AUC of 0.85. Conclusion: Although new MS risk SNPs emerge rapidly, the discriminatory ability in a clinical setting will be limited
Tropomyosin Isoforms Specify Functionally Distinct Actin Filament Populations In Vitro
Actin filaments assemble into a variety of networks to provide force for diverse cellular processes [1]. Tropomyosins are coiled-coil dimers that form head-to-tail polymers along actin filaments and regulate interactions of other proteins, including actin-de polymerizing factor (ADF)/cofilins and myosins, with actin [2-5]. In mammals, >40 tropomyosin isoforms can be generated through alternative splicing from four tropomyosin genes. Different isoforms display non-redundant functions and partially non-overlapping localization patterns, for example within the stress fiber network [6, 7]. Based on cell biological studies, it was thus proposed that tropomyosin isoforms may specify the functional properties of different actin filament populations [2]. To test this hypothesis, we analyzed the properties of actin filaments decorated by stress-fiber-associated tropomyosins (Tpm1.6, Tpm1.7, Tpm2.1, Tpm3.1, Tpm3.2, and Tpm4.2). These proteins bound F-actin with high affinity and competed with a-actinin for actin filament binding. Importantly, total internal reflection fluorescence (TIRF) microscopy of fluorescently tagged proteins revealed that most tropomyosin isoforms cannot co-polymerize with each other on actin filaments. These isoforms also bind actin with different dynamics, which correlate with their effects on actin-binding proteins. The long isoforms Tpm1.6 and Tpm1.7 displayed stable interactions with actin filaments and protected filaments from ADF/cofilin-mediated disassembly, but did not activate non-muscle myosin Ila (NMIIa). In contrast, the short isoforms Tpm3.1, Tpm3.2, and Tpm4.2 displayed rapid dynamics on actin filaments and stimulated the ATPase activity of NMIla, but did not efficiently protect filaments from ADF/cofilin. Together, these data provide experimental evidence that tropomyosin isoforms segregate to different actin filaments and specify functional properties of distinct actin filament populations.Peer reviewe
Antibody to aquaporin-4 in the long-term course of neuromyelitis optica
Neuromyelitis optica (NMO) is a severe inflammatory CNS disorder of putative autoimmune aetiology, which predominantly affects the spinal cord and optic nerves. Recently, a highly specific serum reactivity to CNS microvessels, subpia and Virchow–Robin spaces was described in patients with NMO [called NMO–IgG (NMO–immunoglobulin G)]. Subsequently, aquaporin-4 (AQP4), the most abundant water channel in the CNS, was identified as its target antigen. Strong support for a pathogenic role of the antibody would come from studies demonstrating a correlation between AQP4-Ab (AQP4-antibody) titres and the clinical course of disease. In this study, we determined AQP4-Ab serum levels in 96 samples from eight NMO–IgG positive patients (median follow-up 62 months) in a newly developed fluorescence-based immunoprecipitation assay employing recombinant human AQP4. We found that AQP4-Ab serum levels correlate with clinical disease activity, with relapses being preceded by an up to 3-fold increase in AQP4-Ab titres, which was not paralleled by a rise in other serum autoantibodies in one patient. Moreover, AQP4-Ab titres were found to correlate with CD19 cell counts during therapy with rituximab. Treatment with immunosuppressants such as rituximab, azathioprine and cyclophosphamide resulted in a marked reduction in antibody levels and relapse rates. Our results demonstrate a strong relationship between AQP4-Abs and clinical state, and support the hypothesis that these antibodies are involved in the pathogenesis of NMO
Results from 730 kg days of the CRESST-II Dark Matter Search
The CRESST-II cryogenic Dark Matter search, aiming at detection of WIMPs via
elastic scattering off nuclei in CaWO crystals, completed 730 kg days of
data taking in 2011. We present the data collected with eight detector modules,
each with a two-channel readout; one for a phonon signal and the other for
coincidently produced scintillation light. The former provides a precise
measure of the energy deposited by an interaction, and the ratio of
scintillation light to deposited energy can be used to discriminate different
types of interacting particles and thus to distinguish possible signal events
from the dominant backgrounds. Sixty-seven events are found in the acceptance
region where a WIMP signal in the form of low energy nuclear recoils would be
expected. We estimate background contributions to this observation from four
sources: 1) "leakage" from the e/\gamma-band 2) "leakage" from the
\alpha-particle band 3) neutrons and 4) Pb-206 recoils from Po-210 decay. Using
a maximum likelihood analysis, we find, at a high statistical significance,
that these sources alone are not sufficient to explain the data. The addition
of a signal due to scattering of relatively light WIMPs could account for this
discrepancy, and we determine the associated WIMP parameters.Comment: 17 pages, 13 figure
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