Half-mass radii for ~7,000 galaxies at 1.0 < z < 2.5: most of the evolution in the mass-size relation is due to color gradients

Radial mass-to-light ratio gradients cause the half-mass and half-light radii of galaxies to differ, potentially biasing studies that use half-light radii. Here we present the largest catalog to date of galaxy half-mass radii at z > 1: 7,006 galaxies in the CANDELS fields at 1.0 < z < 2.5. The sample includes both star-forming and quiescent galaxies with stellar masses 9.0 < log(M_* / M_\odot) < 11.5. We test three methods for calculating half-mass radii from multi-band PSF-matched HST imaging: two based on spatially-resolved SED modeling, and one that uses a rest-frame color profile. All three methods agree, with scatter <~0.3 dex. In agreement with previous studies, most galaxies in our sample have negative color gradients (the centers are redder than the outskirts, and r_e,mass < r_e,light). We find that color gradient strength has significant trends with increasing stellar mass, half-light radius, U-V color, and stellar mass surface density. These trends have not been seen before at z>1. Furthermore, color gradients of star-forming and quiescent galaxies show a similar redshift evolution: they are flat at z>~2, then steeply decrease as redshift decreases. This affects the galaxy mass-size relation. The normalizations of the star-forming and quiescent r_mass-M_* relations are 10-40% smaller than the corresponding r_light-M_* relations; the slopes are ~0.1-0.3 dex shallower. Finally, the half-mass radii of star-forming and quiescent galaxies at M_* = 10^{10.5}M_\odot only grow by ~1%$ and ~8% between z~2.25 and z~1.25. This is significantly less than the ~37% and ~47% size increases found when using the half-light radius.Comment: 18 pages, 10 figures. Accepted to Ap

Regulation of nitric oxide signaling by formation of a distal receptor-ligand complex.

The binding of nitric oxide (NO) to the heme cofactor of heme-nitric oxide/oxygen binding (H-NOX) proteins can lead to the dissociation of the heme-ligating histidine residue and yield a five-coordinate nitrosyl complex, an important step for NO-dependent signaling. In the five-coordinate nitrosyl complex, NO can reside on either the distal or proximal side of the heme, which could have a profound influence over the lifetime of the in vivo signal. To investigate this central molecular question, we characterized the Shewanella oneidensis H-NOX (So H-NOX)-NO complex biophysically under limiting and excess NO conditions. The results show that So H-NOX preferably forms a distal NO species with both limiting and excess NO. Therefore, signal strength and complex lifetime in vivo will be dictated by the dissociation rate of NO from the distal complex and the rebinding of the histidine ligand to the heme

Massive quenched galaxies at z~0.7 retain large molecular gas reservoirs

The physical mechanisms that quench star formation, turning blue star-forming galaxies into red quiescent galaxies, remain unclear. In this Letter, we investigate the role of gas supply in suppressing star formation by studying the molecular gas content of post-starburst galaxies. Leveraging the wide area of the SDSS, we identify a sample of massive intermediate-redshift galaxies that have just ended their primary epoch of star formation. We present ALMA CO(2-1) observations of two of these post-starburst galaxies at z~0.7 with M* ~ 2x10^11 Msun. Their molecular gas reservoirs of (6.4 +/- 0.8) x 10^9 Msun and (34.0 +/- 1.6) x 10^9 Msun are an order of magnitude larger than comparable-mass galaxies in the local universe. Our observations suggest that quenching does not require the total removal or depletion of molecular gas, as many quenching models suggest. However, further observations are required both to determine if these apparently quiescent objects host highly obscured star formation and to investigate the intrinsic variation in the molecular gas properties of post-starburst galaxies.Comment: Accepted for publication in ApJ Letters (6 pages, 5 figures

The Width of a CME and the Source of the Driving Magnetic Explosion

We show that the strength of the magnetic field in the area covered by the flare arcade following a CME-producing ejective solar eruption can be estimated from the final angular width of the CME in the outer corona and the final angular width of the flare arcade. We assume (1) the flux-rope plasmoid ejected from the flare site becomes the interior of the CME plasmoid, (2) in the outer corona the CME is roughly a "spherical plasmoid with legs" shaped like a light bulb, and (3) beyond some height in or below the outer corona the CME plasmoid is in lateral pressure balance with the surrounding magnetic field. The strength of the nearly radial magnetic field in the outer corona is estimated from the radial component of the interplanetary magnetic field measured by Ulysses. We apply this model to three well-observed CMEs that exploded from flare regions of extremely different size and magnetic setting. In each event, the estimated source-region field strength is appropriate for the magnetic setting of the flare. This agreement indicates via the model that CMEs (1) are propelled by the magnetic field of the CME plasmoid pushing against the surrounding magnetic field, and (2) can explode from flare regions that are laterally far offset from the radial path of the CME in the outer corona

Platelet polyphosphate induces fibroblast chemotaxis and myofibroblast differentiation

BackgroundPlatelets secrete many pro‐wound healing molecules such as growth factors and cytokines. We found that releasates from activated human platelets induced the differentiation of cultured murine and human fibroblasts into a myofibroblast phenotype. Surprisingly, most of this differentiation‐inducing activity was heat‐stable, suggesting it was not due to the protein component of the releasates. Inorganic polyphosphate is a major constituent of platelet‐dense granules and promotes blood coagulation and inflammation.ObjectivesWe aim to investigate the contribution of polyphosphate on myofibroblast differentiating activity of platelet releasates.MethodsUsing NIH‐3T3 cells and primary human fibroblasts, we examined the effect of human platelet releasates and chemically synthesized polyphosphate on fibroblast differentiation and migration.ResultsWe found that the myofibroblast‐inducing activity of platelet releasates was severely attenuated after incubation with a polyphosphate‐degrading enzyme, and that fibroblasts responded to platelet‐sized polyphosphate by increased levels of α‐smooth muscle actin, stress fibers, and collagen. Furthermore, fibroblasts were chemotactic toward polyphosphate.ConclusionsThese findings indicate that platelet‐derived polyphosphate acts as a cell signaling molecule by inducing murine and human fibroblasts to differentiate into myofibroblasts, a cell type known to drive both wound healing and fibrosing diseases. Polyphosphate therefore not only promotes early wound responses through enhancing fibrin clot formation, but also may play roles in the later stages of wound healing, and, potentially, progression of fibrotic diseases, by recruiting fibroblasts and inducing their differentiation into myofibroblasts.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/163376/2/jth15066_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/163376/1/jth15066.pd