164 research outputs found
Rotational and Cyclical Variability in gamma Cassiopeia
We report results of a nine-year monitoring effort on the unusual classical
Be with a robotic ground-based (APT) B,V-filtered telescope as well as
simultaneous observations in 2004 November with this instrument and the RXTE
(X-ray) telescope. Our observations disclosed no correlated optical response to
the rapid X-ray flares in this star, nor did the star show any sustained flux
changes during the course of either of the two monitored nights in either
wavelength regime. Our optical light curves reveal that gamma Cas undergoes
\~3%-amplitude cycles with lengths of 60--90 days. Over the nine days we
monitored the star with the RXTE, the X-ray flux varied in phase with its
optical cycle and with an amplitude predicted from correlated optical/X-ray
data from an earlier paper. The amplitudes of the V magnitude cycles are
30--40% larger than the B amplitudes, suggesting the seat of the cycles is
circumstellar. The cycle lengths constantly change and can damp or grow on
timescales as short as 13 days. We have also discovered a coherent period of
1.21581 +/-0.00002 days in all our data, which is consistent only with
rotation. The full amplitude of this variation is 0.0060 in both filters. The
derived waveform, somewhat surprisingly, is almost sawtooth in shape. This
variation probably originates on the star's surface. This circumstance hints at
the existence of a strong magnetic field with a complex topology and an
associated heterogeneous surface composition.Comment: 31 pages, 7 figures. Submitted to The Astrophysical Journa
X-ray and Optical Variations in the Classical Be Star gamma Cas
gamma Cas (B0.5e) is known to be a unique X-ray source because ot its
moderate L_x, hard X-ray spectrum, and light curve punctuated by ubiquitous
flares and slow undulations. Its X-ray peculiarities have led to a controversy
concerning their origin: either from wind infall onto a putative degenerate
companion, as for typical Be/X-ray binaries, or from the Be star per se. Recent
progress has been made to address this: (1) the discovery that gamma Cas is an
eccentric binary system (P = 203.59 d) with unknown secondary type, (2) the
accumulation of RXTE data at 9 epochs in 1996-2000, and (3) the collation of
robotic telescope B, V-band photometric observations over 4 seasons. The latter
show a 3%, cyclical flux variation with cycle lengths 55-93 days. We find that
X-ray fluxes at all 9 epochs show random variations with orbital phase. This
contradicts the binary accretion model, which predicts a substantial
modulation. However,these fluxes correlate well with the cyclical optical
variations. Also, the 6 flux measurements in 2000 closely track the
interpolated optical variations between the 2000 and 2001 observing seasons.
Since the optical variations represent a far greater energy than that emitted
as X-rays, the optical variability cannot arise from X-ray reprocessing.
However, the strong correlation between the two suggests that they are driven
by a common mechanism. We propose that this mechanism is a cyclical magnetic
dynamo excited by a Balbus-Hawley instability located within the inner part of
the circumstellar disk. In our model, variations in the field strength directly
produce the changes in the magnetically related X-ray activity. Turbulence
associated with the dynamo results in changes to the density distribution
within the disk and creates the observed optical variations.Comment: 30 dbl-spaced pages, Latex, plus 11 figures. Accepted by Ap
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The relationship between γ Cassiopeiae’s X-ray emission and its circumstellar environment
γ Cas is the prototypical classical Be star and is recently best known for its variable hard X-ray emission. To elucidate the reasons for this emission, we mounted a multiwavelength campaign in 2010 centered around four XMM-Newton observations. The observational techniques included long baseline optical interferometry (LBOI) from two instruments at CHARA, photometry carried out by an automated photometric telescope and Hα observations. Because γ Cas is also known to be in a binary, we measured radial velocities from the Hα line and redetermined its period as 203.55 ± 0.20 days and its eccentricity as near zero. The LBOI observations suggest that the star’s decretion disk was axisymmetric in 2010, has an system inclination angle near 45°, and a larger radius than previously reported. In addition, the Be star began an “outburst” at the beginning of our campaign, made visible by a brightening and reddening of the disk during our campaign and beyond. Our analyses of the new high resolution spectra disclosed many attributes also found from spectra obtained in 2001 (Chandra) and 2004 (XMM-Newton). As well as a dominant hot ( ≈ 14 keV) thermal component, the familiar attributes included: (i) a fluorescent feature of Fe K even stronger than observed at previous times; (ii) strong lines of N VII and Ne XI lines indicative of overabundances; and (iii) a subsolar Fe abundance from K-shell lines but a solar abundance from L-shell ions. We also found that two absorption columns are required to fit the continuum. While the first one maintained its historical average of 1 × 1021 cm-2, the second was very large and doubled to 7.4 × 1023 cm-2 during our X-ray observations. Although we found no clear relation between this column density and orbital phase, it correlates well with the disk brightening and reddening both in the 2010 and earlier observations. Thus, the inference from this study is that much (perhaps all?) of the X-ray emission from this source originates behind matter ejected by γ Cas into our line of sight
MicroRNA‐146 represses endothelial activation by inhibiting pro‐inflammatory pathways
Activation of inflammatory pathways in the endothelium contributes to vascular diseases, including sepsis and atherosclerosis. We demonstrate that miR-146a and miR-146b are induced in endothelial cells upon exposure to pro-inflammatory cytokines. Despite the rapid transcriptional induction of the miR-146a/b loci, which is in part mediated by EGR-3, miR-146a/b induction is delayed and sustained compared to the expression of leukocyte adhesion molecules, and in fact coincides with the down-regulation of inflammatory gene expression. We demonstrate that miR-146 negatively regulates inflammation. Over-expression of miR-146a blunts endothelial activation, while knock-down of miR-146a/b in vitro or deletion of miR-146a in mice has the opposite effect. MiR-146 represses the pro-inflammatory NF-κB pathway as well as the MAP kinase pathway and downstream EGR transcription factors. Finally, we demonstrate that HuR, an RNA binding protein that promotes endothelial activation by suppressing expression of endothelial nitric oxide synthase (eNOS), is a novel miR-146 target. Thus, we uncover an important negative feedback regulatory loop that controls pro-inflammatory signalling in endothelial cells that may impact vascular inflammatory diseases
Short-Term Trends in Bastardy in Taiwan
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68002/2/10.1177_036319908000500303.pd
Genetic Drivers of Heterogeneity in Type 2 Diabetes Pathophysiology
Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P \u3c 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care
Genetic drivers of heterogeneity in type 2 diabetes pathophysiology
Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P < 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.</p
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