The Nearby Neutron Star RX J0720.4-3125 from Radio to X-rays

We present radio, optical, ultraviolet, and X-ray observations of the isolated, thermally-emitting neutron star RX J0720.4-3125 using the Parkes radio telescope, the Very Large Array, the Hubble Space Telescope, and the Chandra X-ray Observatory. From these data we show that the optical/UV spectrum of RX J0720.4-3125 is not well fit by a Rayleigh-Jeans tail as previously thought, but is instead best fit by either a single non-thermal power-law or a combination of a Rayleigh-Jeans tail and a non-thermal power-law. Taken together with the X-ray spectrum, we find the best model for RX J0720.4-3125 to be two blackbodies plus a power-law, with the cool blackbody implying a radius of 11-13 km at an assumed distance of 300 pc. This is similar to many middle aged (10^{5-6} yr) radio pulsars such as PSR B0656+14, evidence supporting the hypothesis that RX J0720.4-3125 is likely to be an off-beam radio pulsar. The radio data limit the flux at 1.4 GHz to be <0.24 mJy, or a luminosity limit of 4*pi*d^2*F < 3e25*d_300^2 ergs/s, and we see no sign of extended nebulosity, consistent with expectations for a pulsar like RX J0720.4-3125.Comment: 13 pages, 9 figures. Uses emulateapj5.sty and onecolfloat5.sty. Accepted for publication in Ap

Mechanistic underpinning of an inside–out concept for autoimmunity in multiple sclerosis

The neuroinflammatory disease multiple sclerosis is driven by autoimmune pathology in the central nervous system. However, the trigger of the autoimmune pathogenic process is unknown. MS models in immunologically naïve, specific‐pathogen‐free bred rodents support an exogenous trigger, such as an infection. The validity of this outside–in pathogenic concept for MS has been frequently challenged by the difficulty to translate pathogenic concepts developed in these models into effective therapies for the MS patient. Studies in well‐validated non‐human primate multiple sclerosis models where, just like in humans, the autoimmune pathogenic process develops from an experienced immune system trained by prior infections, rather support an endogenous trigger. Data reviewed here corroborate the validity of this inside–out pathogenic concept for multiple sclerosis. They also provide a plausible sequence of events reminiscent of Wilkin’s primary lesion theory: (i) that autoimmunity is a physiological response of the immune system against excess antigen turnover in diseased tissue (the primary lesion) and (ii) that individuals developing autoimmune disease are (genetically predisposed) high responders against critical antigens. Data obtained in multiple sclerosis brains reveal the presence in normally appearing white matter of myelinated axons where myelin sheaths have locally dissociated from their enwrapped axon (i.e., blistering). The ensuing disintegration of axon–myelin units potentially causes the excess systemic release of post‐translationally modified myelin. Data obtained in a unique primate multiple sclerosis model revealed a core pathogenic role of T cells present in the normal repertoire, which hyper‐react to post‐translationally modified (citrullinated) myelin–oligodendrocyte glycoprotein and evoke clinical and pathological aspects of multiple sclerosis

A Transiting Planet of a Sun-like Star

A planet transits an 11th magnitude, G1V star in the constellation Corona Borealis. We designate the planet XO-1b, and the star, XO-1, also known as GSC 02041-01657. XO-1 lacks a trigonometric distance; we estimate it to be 200+-20 pc. Of the ten stars currently known to host extrasolar transiting planets, the star XO-1 is the most similar to the Sun in its physical characteristics: its radius is 1.0+-0.08 R_Sun, its mass is 1.0+-0.03 M_Sun, V sini < 3 km/s, and its metallicity [Fe/H] is 0.015+-0.04. The orbital period of the planet XO-1b is 3.941534+-0.000027 days, one of the longer ones known. The planetary mass is 0.90+-0.07 M_Jupiter, which is marginally larger than that of other transiting planets with periods between 3 and 4 days. Both the planetary radius and the inclination are functions of the spectroscopically determined stellar radius. If the stellar radius is 1.0+-0.08 R_Sun, then the planetary radius is 1.30+-0.11 R_Jupiter and the inclination of the orbit is 87.7+-1.2 degrees. We have demonstrated a productive international collaboration between professional and amateur astronomers that was important to distinguishing this planet from many other similar candidates.Comment: 31 pages, 9 figures, accepted for part 1 of Ap

The XO Project: Searching for Transiting Extra-solar Planet Candidates

The XO project's first objective is to find hot Jupiters transiting bright stars, i.e. V < 12, by precision differential photometry. Two XO cameras have been operating since September 2003 on the 10,000-foot Haleakala summit on Maui. Each XO camera consists of a 200-mm f/1.8 lens coupled to a 1024x1024 pixel, thinned CCD operated by drift scanning. In its first year of routine operation, XO has observed 6.6% of the sky, within six 7 deg-wide strips scanned from 0 deg to +63 deg of declination and centered at RA=0, 4, 8, 12, 16, and 20 hours. Autonomously operating, XO records 1 billion pixels per clear night, calibrates them photometrically and astrometrically, performs aperture photometry, archives the pixel data and transmits the photometric data to STScI for further analysis. From the first year of operation, the resulting database consists of photometry of 100,000 stars at more than 1000 epochs per star with differential photometric precision better than 1% per epoch. Analysis of the light curves of those stars produces transiting-planet candidates requiring detailed follow up, described elsewhere, culminating in spectroscopy to measure radial-velocity variation in order to differentiate genuine planets from the more numerous impostors, primarily eclipsing binary and multiple stars.Comment: 29 pages, 12 figures, accepted by PASP for Aug 2005 issu

XO-2b: Transiting Hot Jupiter in a Metal-rich Common Proper Motion Binary

We report on a V=11.2 early K dwarf, XO-2 (GSC 03413-00005), that hosts a Rp=0.98+0.03/-0.01 Rjup, Mp=0.57+/-0.06 Mjup transiting extrasolar planet, XO-2b, with an orbital period of 2.615857+/-0.000005 days. XO-2 has high metallicity, [Fe/H]=0.45+/-0.02, high proper motion, mu_tot=157 mas/yr, and has a common proper motion stellar companion with 31" separation. The two stars are nearly identical twins, with very similar spectra and apparent magnitudes. Due to the high metallicity, these early K dwarf stars have a mass and radius close to solar, Ms=0.98+/-0.02 Msolar and Rs=0.97+0.02/-0.01 Rsolar. The high proper motion of XO-2 results from an eccentric orbit (Galactic pericenter, Rper<4 kpc) well confined to the Galactic disk (Zmax~100 pc). In addition, the phase space position of XO-2 is near the Hercules dynamical stream, which points to an origin of XO-2 in the metal-rich, inner Thin Disk and subsequent dynamical scattering into the solar neighborhood. We describe an efficient Markov Chain Monte Carlo algorithm for calculating the Bayesian posterior probability of the system parameters from a transit light curve.Comment: 14 pages, 10 Figures, Accepted in ApJ. Negligible changes to XO-2 system properties. Removed Chi^2 light curve analysis section, and simplified MCMC light curve analysis discussio

A T-type channel-calmodulin complex triggers αCaMKII activation

Abstract Calmodulin (CaM) is an important signaling molecule that regulates a vast array of cellular functions by activating second messengers involved in cell function and plasticity. Low voltage-activated calcium channels of the Cav3 family have the important role of mediating low threshold calcium influx, but were not believed to interact with CaM. We find a constitutive association between CaM and the Cav3.1 channel at rest that is lost through an activity-dependent and Cav3.1 calcium-dependent CaM dissociation. Moreover, Cav3 calcium influx is sufficient to activate αCaMKII in the cytoplasm in a manner that depends on an intact Cav3.1 C-terminus needed to support the CaM interaction. Our findings thus establish that T-type channel calcium influx invokes a novel dynamic interaction between CaM and Cav3.1 channels to trigger a signaling cascade that leads to αCaMKII activation

Hot subdwarfs from the ESO Supernova Ia Progenitor Survey: II. Atmospheric parameters of subdwarf O stars

We address the origin and evolutionary status of hot subdwarf stars by studying the optical spectral properties of 58 subdwarf O (sdO) stars. Combining them with the results of our previously studied subdwarf B (sdB) stars, we aim at investigating possible evolutionary links. We analyze high-resolution ESO VLT UVES spectra from the ESO Supernova Ia Progenitor Survey (SPY). Effective temperatures, gravities, and helium abundances are determined simultaneously by fitting the profiles of H and He lines using dedicated synthetic spectra in NLTE. Evidence for cool companions to 8 sdOs as well as a binary consisting of two sdO stars is found. A correlation between He abundances and the presence of carbon and/or nitrogen lines emerges: below solar He abundance, no sdO shows C or N lines. In contrast, C and/or N lines are present in ALL sdOs with super- solar He abundance. We thus use the solar He abundance to divide our sample into He-deficient and He-enriched sdOs. While He-deficient sdOs are scattered in a wide range of the Teff-log(g)-diagram, most of the He-enriched sdOs cluster in a narrow region at Teff = 40,000 ... 50,000K and log(g)=5.5 ... 6.0. An evolu- tionary link between sdBs and sdOs appears plausible only for the He-deficient sdOs indicating that they are the likely successors to sdBs. The properties of He-enriched sdOs cannot be explained with canonical single star evolutionary models. Alternative scenarios (late hot flasher) as well as for binary evolution (white dwarf merger; post-RGB evolution) are tested. While we regard the post-RGB scenario as inappropriate, the white dwarf merger and the late hot flasher scenarios remain viable to explain the origin of He-enriched sdOs.Comment: 14 pages, 10 figures, Astronomy & Astrophysics accepte

Diagnosing Alzheimer's Disease from Circulating Blood Leukocytes Using a Fluorescent Amyloid Probe

BACKGROUND: Toxic amyloid-β (Aβ) peptides aggregate into higher molecular weight assemblies and accumulate not only in the extracellular space, but also in the walls of blood vessels in the brain, increasing their permeability, and promoting immune cell migration and activation. Given the prominent role of the immune system, phagocytic blood cells may contact pathological brain materials. OBJECTIVE: To develop a novel method for early Alzheimer's disease (AD) detection, we used blood leukocytes, that could act as "sentinels" after trafficking through the brain microvasculature, to detect pathological amyloid by labelling with a conformationally-sensitive fluorescent amyloid probe and imaging with confocal spectral microscopy. METHODS: Formalin-fixed peripheral blood mononuclear cells (PBMCs) from cognitively healthy control (HC) subjects, mild cognitive impairment (MCI) and AD patients were stained with the fluorescent amyloid probe K114, and imaged. Results were validated against cerebrospinal fluid (CSF) biomarkers and clinical diagnosis. RESULTS: K114-labeled leukocytes exhibited distinctive fluorescent spectral signatures in MCI/AD subjects. Comparing subjects with single CSF biomarker-positive AD/MCI to negative controls, our technique yielded modest AUCs, which improved to the 0.90 range when only MCI subjects were included in order to measure performance in an early disease state. Combining CSF Aβ 42 and t-Tau metrics further improved the AUC to 0.93. CONCLUSION: Our method holds promise for sensitive detection of AD-related protein misfolding in circulating leukocytes, particularly in the early stages of disease

PLoS Genet.

The expansion of CAG/CTG repeats is responsible for many diseases, including Huntington's disease (HD) and myotonic dystrophy 1. CAG/CTG expansions are unstable in selective somatic tissues, which accelerates disease progression. The mechanisms underlying repeat instability are complex, and it remains unclear whether chromatin structure and/or transcription contribute to somatic CAG/CTG instability in vivo. To address these issues, we investigated the relationship between CAG instability, chromatin structure, and transcription at the HD locus using the R6/1 and R6/2 HD transgenic mouse lines. These mice express a similar transgene, albeit integrated at a different site, and recapitulate HD tissue-specific instability. We show that instability rates are increased in R6/2 tissues as compared to R6/1 matched-samples. High transgene expression levels and chromatin accessibility correlated with the increased CAG instability of R6/2 mice. Transgene mRNA and H3K4 trimethylation at the HD locus were increased, whereas H3K9 dimethylation was reduced in R6/2 tissues relative to R6/1 matched-tissues. However, the levels of transgene expression and these specific histone marks were similar in the striatum and cerebellum, two tissues showing very different CAG instability levels, irrespective of mouse line. Interestingly, the levels of elongating RNA Pol II at the HD locus, but not the initiating form of RNA Pol II, were tissue-specific and correlated with CAG instability levels. Similarly, H3K36 trimethylation, a mark associated with transcription elongation, was specifically increased at the HD locus in the striatum and not in the cerebellum. Together, our data support the view that transcription modulates somatic CAG instability in vivo. More specifically, our results suggest for the first time that transcription elongation is regulated in a tissue-dependent manner, contributing to tissue-selective CAG instability.The following values have no corresponding Zotero field:alt-title: PLoS Genet.number: 11remote-database-provider: PubMe