Estimating magnetic filling factors from simultaneous spectroscopy and photometry : disentangling spots, plage, and network

A.C.C. acknowledges support from the Science and Technology Facilities Council (STFC) consolidated grant number ST/R000824/1.State-of-the-art radial velocity (RV) exoplanet searches are limited by the effects of stellar magnetic activity. Magnetically active spots, plage, and network regions each have different impacts on the observed spectral lines and therefore on the apparent stellar RV. Differentiating the relative coverage, or filling factors, of these active regions is thus necessary to differentiate between activity-driven RV signatures and Doppler shifts due to planetary orbits. In this work, we develop a technique to estimate feature-specific magnetic filling factors on stellar targets using only spectroscopic and photometric observations. We demonstrate linear and neural network implementations of our technique using observations from the solar telescope at HARPS-N, the HK Project at the Mt. Wilson Observatory, and the Total Irradiance Monitor onboard SORCE. We then compare the results of each technique to direct observations by the Solar Dynamics Observatory. Both implementations yield filling factor estimates that are highly correlated with the observed values. Modeling the solar RVs using these filling factors reproduces the expected contributions of the suppression of convective blueshift and rotational imbalance due to brightness inhomogeneities. Both implementations of this technique reduce the overall activity-driven rms RVs from 1.64 to 1.02 m s(-1), corresponding to a 1.28 m s(-1) reduction in the rms variation. The technique provides an additional 0.41 m s(-1) reduction in the rms variation compared to traditional activity indicators.PostprintPeer reviewe

Detection Limits of Low-mass, Long-period Exoplanets Using Gaussian Processes Applied to HARPS-N Solar Radial Velocities

Radial velocity (RV) searches for Earth-mass exoplanets in the habitable zone around Sun-like stars are limited by the effects of stellar variability on the host star. In particular, suppression of convective blueshift and brightness inhomogeneities due to photospheric faculae/plage and starspots are the dominant contribution to the variability of such stellar RVs. Gaussian process (GP) regression is a powerful tool for statistically modeling these quasi-periodic variations. We investigate the limits of this technique using 800 days of RVs from the solar telescope on the High Accuracy Radial velocity Planet Searcher for the Northern hemisphere (HARPS-N) spectrograph. These data provide a well-sampled time series of stellar RV variations. Into this data set, we inject Keplerian signals with periods between 100 and 500 days and amplitudes between 0.6 and 2.4 ms−1. We use GP regression to fit the resulting RVs and determine the statistical significance of recovered periods and amplitudes. We then generate synthetic RVs with the same covariance properties as the solar data to determine a lower bound on the observational baseline necessary to detect low-mass planets in Venus-like orbits around a Sun-like star. Our simulations show that discovering planets with a larger mass (∼0.5 ms−1) using current-generation spectrographs and GP regression will require more than 12 yr of densely sampled RV observations. Furthermore, even with a perfect model of stellar variability, discovering a true exo-Venus (∼0.1 m s −1 ) with current instruments would take over 15 yr. Therefore, next-generation spectrographs and better models of stellar variability are required for detection of such planets

Detection Limits of Low-mass, Long-period Exoplanets Using Gaussian Processes Applied to HARPS-N Solar Radial Velocities

Radial velocity (RV) searches for Earth-mass exoplanets in the habitable zone around Sun-like stars are limited by the effects of stellar variability on the host star. In particular, suppression of convective blueshift and brightness inhomogeneities due to photospheric faculae/plage and starspots are the dominant contribution to the variability of such stellar RVs. Gaussian process (GP) regression is a powerful tool for statistically modeling these quasi-periodic variations. We investigate the limits of this technique using 800 days of RVs from the solar telescope on the High Accuracy Radial velocity Planet Searcher for the Northern hemisphere (HARPS-N) spectrograph. These data provide a well-sampled time series of stellar RV variations. Into this data set, we inject Keplerian signals with periods between 100 and 500 days and amplitudes between 0.6 and 2.4 m s$^{-1}$. We use GP regression to fit the resulting RVs and determine the statistical significance of recovered periods and amplitudes. We then generate synthetic RVs with the same covariance properties as the solar data to determine a lower bound on the observational baseline necessary to detect low-mass planets in Venus-like orbits around a Sun-like star. Our simulations show that discovering planets with a larger mass ($\sim$ 0.5 m s$^{-1}$) using current-generation spectrographs and GP regression will require more than 12 yr of densely sampled RV observations. Furthermore, even with a perfect model of stellar variability, discovering a true exo-Venus ($\sim$ 0.1 m s$^{-1}$) with current instruments would take over 15 yr. Therefore, next-generation spectrographs and better models of stellar variability are required for detection of such planets

Activation of Regulatory T Cells during Inflammatory Response Is Not an Exclusive Property of Stem Cells

BACKGROUND: Sepsis and systemic-inflammatory-response-syndrome (SIRS) remain major causes for fatalities on intensive care units despite up-to-date therapy. It is well accepted that stem cells have immunomodulatory properties during inflammation and sepsis, including the activation of regulatory T cells and the attenuation of distant organ damage. Evidence from recent work suggests that these properties may not be exclusively attributed to stem cells. This study was designed to evaluate the immunomodulatory potency of cellular treatment during acute inflammation in a model of sublethal endotoxemia and to investigate the hypothesis that immunomodulations by cellular treatment during inflammatory response is not stem cell specific. METHODOLOGY/PRINCIPAL FINDINGS: Endotoxemia was induced via intra-peritoneal injection of lipopolysaccharide (LPS) in wild type mice (C3H/HeN). Mice were treated with either vital or homogenized amniotic fluid stem cells (AFS) and sacrificed for specimen collection 24 h after LPS injection. Endpoints were plasma cytokine levels (BD™ Cytometric Bead Arrays), T cell subpopulations (flow-cytometry) and pulmonary neutrophil influx (immunohistochemistry). To define stem cell specific effects, treatment with either vital or homogenized human-embryonic-kidney-cells (HEK) was investigated in a second subset of experiments. Mice treated with homogenized AFS cells showed significantly increased percentages of regulatory T cells and Interleukin-2 as well as decreased amounts of pulmonary neutrophils compared to saline-treated controls. These results could be reproduced in mice treated with vital HEK cells. No further differences were observed between plasma cytokine levels of endotoxemic mice. CONCLUSIONS/SIGNIFICANCE: The results revealed that both AFS and HEK cells modulate cellular immune response and distant organ damage during sublethal endotoxemia. The observed effects support the hypothesis, that immunomodulations are not exclusive attributes of stem cells

Estrogen Prevents Oxidative Damage to the Mitochondria in Friedreich's Ataxia Skin Fibroblasts

Estrogen and estrogen-related compounds have been shown to have very potent cytoprotective properties in a wide range of disease models, including an in vitro model of Friedreich's ataxia (FRDA). This study describes a potential estrogen receptor (ER)-independent mechanism by which estrogens act to protect human FRDA skin fibroblasts from a BSO-induced oxidative insult resulting from inhibition of de novo glutathione (GSH) synthesis. We demonstrate that phenolic estrogens, independent of any known ER, are able to prevent lipid peroxidation and mitochondrial membrane potential (ΔΨm) collapse, maintain ATP at near control levels, increase oxidative phosphorylation and maintain activity of aconitase. Estrogens did not, however, prevent BSO from depleting GSH or induce an increased expression level of GSH. The cytoprotective effects of estrogen appear to be due to a direct overall reduction in oxidative damage to the mitochondria, enabling the FRDA fibroblast mitochondria to generate sufficient ATP for energy requirements and better survive oxidative stress. These data support the hypothesis that phenol ring containing estrogens are possible candidate drugs for the delay and/or prevention of FRDA symptoms

Extent of Structural Asymmetry in Homodimeric Proteins: Prevalence and Relevance

Most homodimeric proteins have symmetric structure. Although symmetry is known to confer structural and functional advantage, asymmetric organization is also observed. Using a non-redundant dataset of 223 high-resolution crystal structures of biologically relevant homodimers, we address questions on the prevalence and significance of asymmetry. We used two measures to quantify global and interface asymmetry, and assess the correlation of several molecular and structural parameters with asymmetry. We have identified rare cases (11/223) of biologically relevant homodimers with pronounced global asymmetry. Asymmetry serves as a means to bring about 2∶1 binding between the homodimer and another molecule; it also enables cellular signalling arising from asymmetric macromolecular ligands such as DNA. Analysis of these cases reveals two possible mechanisms by which possible infinite array formation is prevented. In case of homodimers associating via non-topologically equivalent surfaces in their tertiary structures, ligand-dependent mechanisms are used. For stable dimers binding via large surfaces, ligand-dependent structural change regulates polymerisation/depolymerisation; for unstable dimers binding via smaller surfaces that are not evolutionarily well conserved, dimerisation occurs only in the presence of the ligand. In case of homodimers associating via interaction surfaces with parts of the surfaces topologically equivalent in the tertiary structures, steric hindrance serves as the preventive mechanism of infinite array. We also find that homodimers exhibiting grossly symmetric organization rarely exhibit either perfect local symmetry or high local asymmetry. Binding of small ligands at the interface does not cause any significant variation in interface asymmetry. However, identification of biologically relevant interface asymmetry in grossly symmetric homodimers is confounded by the presence of similar small magnitude changes caused due to artefacts of crystallisation. Our study provides new insights regarding accommodation of asymmetry in homodimers

The C. elegans Opa1 Homologue EAT-3 Is Essential for Resistance to Free Radicals

The C. elegans eat-3 gene encodes a mitochondrial dynamin family member homologous to Opa1 in humans and Mgm1 in yeast. We find that mutations in the C. elegans eat-3 locus cause mitochondria to fragment in agreement with the mutant phenotypes observed in yeast and mammalian cells. Electron microscopy shows that the matrices of fragmented mitochondria in eat-3 mutants are divided by inner membrane septae, suggestive of a specific defect in fusion of the mitochondrial inner membrane. In addition, we find that C. elegans eat-3 mutant animals are smaller, grow slower, and have smaller broodsizes than C. elegans mutants with defects in other mitochondrial fission and fusion proteins. Although mammalian Opa1 is antiapoptotic, mutations in the canonical C. elegans cell death genes ced-3 and ced-4 do not suppress the slow growth and small broodsize phenotypes of eat-3 mutants. Instead, the phenotypes of eat-3 mutants are consistent with defects in oxidative phosphorylation. Moreover, eat-3 mutants are hypersensitive to paraquat, which promotes damage by free radicals, and they are sensitive to loss of the mitochondrial superoxide dismutase sod-2. We conclude that free radicals contribute to the pathology of C. elegans eat-3 mutants