The End of the Lines for OX 169: No Binary Broad-Line Region

We show that unusual Balmer emission line profiles of the quasar OX 169, frequently described as either self-absorbed or double peaked, are actually neither. The effect is an illusion resulting from two coincidences. First, the forbidden lines are quite strong and broad. Consequently, the [N II]6583 line and the associated narrow-line component of H-alpha present the appearance of twin H-alpha peaks. Second, the redshift of 0.2110 brings H-beta into coincidence with Na I D at zero redshift, and ISM absorption in Na I D divides the H-beta emission line. In spectra obtained over the past decade, we see no substantial change in the character of the line profiles, and no indication of intrinsic double-peaked structure. The H-gamma, Mg II, and Ly-alpha emission lines are single peaked, and all of the emission-line redshifts are consistent once they are correctly attributed to their permitted and forbidden-line identifications. A systematic shift of up to 700 km/s between broad and narrow lines is seen, but such differences are common, and could be due to gravitational and transverse redshift in a low-inclination disk. Stockton & Farnham (1991) had called attention to an apparent tidal tail in the host galaxy of OX 169, and speculated that a recent merger had supplied the nucleus with a coalescing pair of black holes which was now revealing its existence in the form of two physically distinct broad-line regions. Although there is no longer any evidence for two broad emission-line regions in OX 169, binary black holes should form frequently in galaxy mergers, and it is still worthwhile to monitor the radial velocities of emission lines which could supply evidence of their existence in certain objects.Comment: 19 pages, 5 figures, accepted for publication in Ap.

The Circumstellar Disk of HD 141569 Imaged with NICMOS

Coronagraphic imaging with the Near Infrared Camera and Multi Object Spectrometer on the Hubble Space Telescope reveals a large, ~400 AU (4'') radius, circumstellar disk around the Herbig Ae/Be star HD 141569. A reflected light image at 1.1 micron shows the disk oriented at a position angle of 356 +/- 5 deg and inclined to our line of sight by 51 +/- 3 deg; the intrinsic scattering function of the dust in the disk makes the side inclined toward us, the eastern side, brighter. The disk flux density peaks 185 AU (1.''85) from the star and falls off to both larger and smaller radii. A region of depleted material, or a gap, in the disk is centered 250 AU from the star. The dynamical effect of one or more planets may be necessary to explain this morphology.Comment: 4 pages, LaTeX with emulateapj.sty and epsfig.sty, 4 postscript figures, Accepted to ApJ Letter

On the Origin of Broad Fe K alpha and Hi H alpha Lines in AGN

We examine the properties of the Fe emission lines that arise near 6.4 keV in the ASCA spectra of AGN. Our emphasis is on the Seyfert 1 galaxies where broad and apparently complex Fe K alpha emission is observed. We consider various origins for the line but focus on the pros and cons for line emitting accretion disk models. We develop a simple model of an illuminated disk capable of producing both X-ray and optical lines from a disk. The model is able to reproduce the observed Fe K alpha FWHM ratio as well as the radii of maximum emissivity implied by the profile redshifts. The overall profile shapes however do not fit well the predictions of our disk illumination model nor do we derive always consistent disk inclinations for the two lines. We conclude that the evidence for and against an accretion disk origin for the Fe K alpha emission is equal at best. The bulk of the data requires a very disparate set of line fits which shed little light on a coherent physical model. We briefly consider alternatives to disk emission models and show that a simple bicone model can reproduce the FE line profiles equally well.Comment: 29 pages, 6 tables, 6 figures. Submitted for publication in the Astrophysical Journal part

The Social and Political Dimensions of the Ebola Response: Global Inequality, Climate Change, and Infectious Disease

The 2014 Ebola crisis has highlighted public-health vulnerabilities in Liberia, Sierra Leone, and Guinea – countries ravaged by extreme poverty, deforestation and mining-related disruption of livelihoods and ecosystems, and bloody civil wars in the cases of Liberia and Sierra Leone. Ebola’s emergence and impact are grounded in the legacy of colonialism and its creation of enduring inequalities within African nations and globally, via neoliberalism and the Washington Consensus. Recent experiences with new and emerging diseases such as SARS and various strains of HN influenzas have demonstrated the effectiveness of a coordinated local and global public health and education-oriented response to contain epidemics. To what extent is international assistance to fight Ebola strengthening local public health and medical capacity in a sustainable way, so that other emerging disease threats, which are accelerating with climate change, may be met successfully? This chapter considers the wide-ranging socio-political, medical, legal and environmental factors that have contributed to the rapid spread of Ebola, with particular emphasis on the politics of the global and public health response and the role of gender, social inequality, colonialism and racism as they relate to the mobilization and establishment of the public health infrastructure required to combat Ebola and other emerging diseases in times of climate change

Soil Organic Carbon and Nitrogen Feedbacks on Crop Yields under Climate Change

Articles in A&EL are published under the CC-BY NC ND (non-commercial; no derivatives) license (https://creativecommons.org/licenses/by-nc-nd/2.0/). Users are free to copy and redistribute the material in any medium or format. Any further publication of the article will require proper attribution; no derivative works may be made from this article; and the article may not be used for any commercial gain (https://creativecommons.org/licenses/by-nc-nd/2.0/). The author is given explicit permission to publish the final article in her/his institutional repository. There is an option for the CC-BY license if required by an author's institution.Peer reviewedPublisher PD

Neurobiological Mechanisms That Contribute to Stress-related Cocaine Use

The ability of stressful life events to trigger drug use is particularly problematic for the management of cocaine addiction due to the unpredictable and often uncontrollable nature of stress. For this reason, understanding the neurobiological processes that contribute to stress-related drug use is important for the development of new and more effective treatment strategies aimed at minimizing the role of stress in the addiction cycle. In this review we discuss the neurocircuitry that has been implicated in stress-induced drug use with an emphasis on corticotropin releasing factor actions in the ventral tegmental area (VTA) and an important pathway from the bed nucleus of the stria terminalis to the VTA that is regulated by norepinephrine via actions at beta adrenergic receptors. In addition to the neurobiological mechanisms that underlie stress-induced cocaine seeking, we review findings suggesting that the ability of stressful stimuli to trigger cocaine use emerges and intensifies in an intake-dependent manner with repeated cocaine self-administration. Further, we discuss evidence that the drug-induced neuroadaptations that are necessary for heightened susceptibility to stress-induced drug use are reliant on elevated levels of glucocorticoid hormones at the time of cocaine use. Finally, the potential ability of stress to function as a “stage setter” for drug use – increasing sensitivity to cocaine and drug-associated cues – under conditions where it does not directly trigger cocaine seeking is discussed. As our understanding of the mechanisms through which stress promotes drug use advances, the hope is that so too will the available tools for effectively managing addiction, particularly in cocaine addicts whose drug use is stress-driven

The effect of low-level thin arctic clouds on shortwave irradiance: evaluation of estimates from spaceborne passive imagery with aircraft observations

Cloud optical properties such as optical thickness along with surface albedo are important inputs for deriving the shortwave radiative effects of clouds from spaceborne remote sensing. Owing to insufficient knowledge about the snow or ice surface in the Arctic, cloud detection and the retrieval products derived from passive remote sensing, such as from the Moderate Resolution Imaging Spectroradiometer (MODIS), are difficult to obtain with adequate accuracy&nbsp;&ndash; especially for low-level thin clouds, which are ubiquitous in the Arctic. This study aims at evaluating the spectral and broadband irradiance calculated from MODIS-derived cloud properties in the Arctic using aircraft measurements collected during the Arctic Radiation-IceBridge Sea and Ice Experiment (ARISE), specifically using the upwelling and downwelling shortwave spectral and broadband irradiance measured by the Solar Spectral Flux Radiometer (SSFR) and the BroadBand Radiometer system (BBR). This starts with the derivation of surface albedo from SSFR and BBR, accounting for the heterogeneous surface in the marginal ice zone (MIZ) with aircraft camera imagery, followed by subsequent intercomparisons of irradiance measurements and radiative transfer calculations in the presence of thin clouds. It ends with an attribution of any biases we found to causes, based on the spectral dependence and the variations in the measured and calculated irradiance along the flight track. The spectral surface albedo derived from the airborne radiometers is consistent with prior ground-based and airborne measurements and adequately represents the surface variability for the study region and time period. Somewhat surprisingly, the primary error in MODIS-derived irradiance fields for this study stems from undetected clouds, rather than from the retrieved cloud properties. In our case study, about 27&thinsp;% of clouds remained undetected, which is attributable to clouds with an optical thickness of less than 0.5. We conclude that passive imagery has the potential to accurately predict shortwave irradiances in the region if the detection of thin clouds is improved. Of at least equal importance, however, is the need for an operational imagery-based surface albedo product for the polar regions that adequately captures its temporal, spatial, and spectral variability to estimate cloud radiative effects from spaceborne remote sensing. &nbsp;</p

Mast cell tryptase stimulates myoblast proliferation; a mechanism relying on protease-activated receptor-2 and cyclooxygenase-2

<p>Abstract</p> <p>Background</p> <p>Mast cells contribute to tissue repair in fibrous tissues by stimulating proliferation of fibroblasts through the release of tryptase which activates protease-activated receptor-2 (PAR-2). The possibility that a tryptase/PAR-2 signaling pathway exists in skeletal muscle cell has never been investigated. The aim of this study was to evaluate whether tryptase can stimulate myoblast proliferation and determine the downstream cascade.</p> <p>Methods</p> <p>Proliferation of L6 rat skeletal myoblasts stimulated with PAR-2 agonists (tryptase, trypsin and SLIGKV) was assessed. The specificity of the tryptase effect was evaluated with a specific inhibitor, APC-366. Western blot analyses were used to evaluate the expression and functionality of PAR-2 receptor and to assess the expression of COX-2. COX-2 activity was evaluated with a commercial activity assay kit and by measurement of PGF₂α production. Proliferation assays were also performed in presence of different prostaglandins (PGs).</p> <p>Results</p> <p>Tryptase increased L6 myoblast proliferation by 35% above control group and this effect was completely inhibited by APC-366. We confirmed the expression of PAR-2 receptor <it>in vivo </it>in skeletal muscle cells and in satellite cells and <it>in vitro </it>in L6 cells, where PAR-2 was found to be functional. Trypsin and SLIGKV increased L6 cells proliferation by 76% and 26% above control, respectively. COX-2 activity was increased following stimulation with PAR-2 agonist but its expression remained unchanged. Inhibition of COX-2 activity by NS-398 abolished the stimulation of cell proliferation induced by tryptase and trypsin. Finally, 15-deoxy-Δ-^12,14-prostaglandin J₂(15Δ-PGJ₂), a product of COX-2-derived prostaglandin D₂, stimulated myoblast proliferation, but not PGE₂and PGF₂α.</p> <p>Conclusions</p> <p>Taken together, our data show that tryptase can stimulate myoblast proliferation and this effect is part of a signaling cascade dependent on PAR-2 activation and on the downstream activation of COX-2.</p

Force spectroscopy in studying infection

Biophysical force spectroscopy tools - for example optical tweezers, magnetic tweezers, atomic force microscopy, - have been used to study elastic, mechanical, conformational and dynamic properties of single biological specimens from single proteins to whole cells to reveal information not accessible by ensemble average methods such as X-ray crystallography, mass spectroscopy, gel electrophoresis and so on. Here we review the application of these tools on a range of infection-related questions from antibody-inhibited protein processivity to virus-cell adhesion. In each case we focus on how the instrumental design tailored to the biological system in question translates into the functionality suitable for that particular study. The unique insights that force spectroscopy has gained to complement knowledge learned through population averaging techniques in interrogating biomolecular details prove to be instrumental in therapeutic innovations such as those in structure-based drug design