Modelling the Interstellar Medium of Low Surface Brightness Galaxies: Constraining Internal Extinction, Disk Color Gradients, and Intrinsic Rotation Curve Shapes

We use a combination of three-dimensional Monte Carlo radiative transfer techniques and multi-wavelength (BRHK,H alpha) imaging data to investigate the nature of the interstellar medium (ISM) in the edge-on, low surface brightness (LSB) galaxy UGC7321. Using realistic models that incorporate multiple scattering effects and clumping of the stars and the interstellar material, we explore the distribution and opacity of the interstellar material (gas+dust), and its effects on the observed stellar disk luminosity profiles, color gradients, and rotation curve shape. We find that UGC7321 contains a small but non-negligible dusty component to its ISM, yielding a B-band optical depth tau_e,B~4.0 from disk edge to center. A significant fraction (~50+/-10%) of the interstellar material in the innermost regions of UGC7321 appears to be contained in a clumpy medium, indicating that LSB galaxies can support a modest, multi-phase ISM structure. In spite of the clear presence of dust, we conclude that the large radial optical color gradients observed in UGC7321 and other similar LSB spiral galaxies cannot be accounted for by dust and must result primarily from significant stellar population and/or metallicity gradients. We show that realistic optical depth effects will have little impact on the observed rotation curves of edge-on disk galaxies and cannot explain the linear, slowly rising rotation curves seen in some edge-on LSB spirals. Projection effects create a far larger uncertainty in recovering the true underlying rotation curve shape of galaxies viewed at inclinations i>85 degrees.Comment: accepted to ApJ; 16 pages, 2 tables, and 18 figures; uses emulateapj.st

Dust in the Small Magellanic Cloud: Interstellar Polarization and Extinction

To elucidate the dust properties in the SMC we have for the first time measured linear polarization in five colors in the optical region of the spectrum for a sample of reddened stars. For two of these stars, for which there were no existing UV spectrophotometric measurements, but for which we measured a relatively large polarization, we have also obtained data from the International Ultraviolet Explorer (IUE) in order to study the extinction. The main results are: (1) the wavelength of maximum polarization, $\lambda_{max}$, in the SMC is typically smaller than that in the Galaxy; (2) however, AZV 456, which shows the UV extinction bump, has a $\lambda_{max}$ typical of that in the Galaxy, its polarization curve is narrower, its bump is shifted to shorter wavelengths as compared to the Galaxy and its UV extinction does not conform to the Galactic analytical interpolation curve based on the ratio of total to selective extinction; (3) the 'typical', monotonic SMC extinction curve can be best fit with amorphous carbon and silicate grains; (4) the extinction towards AZV456 may only be explained by assuming a larger gas-to-dust ratio than the observed N(HI)/A(V) value, with a small amount of the available carbon in graphite form; (5) from an analysis of both the extinction and polarization data and our model fits it appears that the SMC has typically smaller grains than those in the Galaxy.Comment: To appear in the ApJ, 50 pages, latex fil

An alginate-layer technique for culture of Brassica oleracea L. protoplasts

Ten accessions belonging to the Brassica oleracea subspecies alba and rubra, and to B. oleracea var. sabauda were used in this study. Protoplasts were isolated from leaves and hypocotyls of in vitro grown plants. The influence of selected factors on the yield, viability, and mitotic activity of protoplasts immobilized in calcium alginate layers was investigated. The efficiency of protoplast isolation from hypocotyls was lower (0.7 ± 0.1 × 106 ml−1) than for protoplasts isolated from leaf mesophyll tissue (2 ± 0.1 × 106 ml−1). High (70–90%) viabilities of immobilized protoplasts were recorded, independent of the explant sources. The highest proportion of protoplasts undergoing divisions was noted for cv. Reball F1, both from mesophyll (29.8 ± 2.2%) and hypocotyl (17.5 ± 0.3%) tissues. Developed colonies of callus tissue were subjected to regeneration and as a result plants from six accessions were obtained

DNA microarray revealed and RNAi plants confirmed key genes conferring low Cd accumulation in barley grains

List of genes down-regulated in both W6nk2 and Zhenong8 after 15 days exposure to 5 ΟM Cd. (DOC 130 kb

How Metabolic State May Regulate Fear: Presence of Metabolic Receptors in the Fear Circuitry

Metabolic status impacts on the emotional brain to induce behavior that maintains energy balance. While hunger suppresses the fear circuitry to promote explorative food-seeking behavior, satiety or obesity may increase fear to prevent unnecessary risk-taking. Here we aimed to unravel which metabolic factors, that transfer information about the acute and the chronic metabolic status, are of primary importance to regulate fear, and to identify their sites of action within fear-related brain regions. We performed a de novo analysis of central and peripheral metabolic factors that can penetrate the blood–brain barrier using genome-wide expression data across the mouse brain from the Allen Brain Atlas (ABA). The central fear circuitry, as defined by subnuclei of the amygdala, the afferent hippocampus, the medial prefrontal cortex and the efferent periaqueductal gray, was enriched with metabolic receptors. Some of their corresponding ligands were known to modulate fear (e.g., estrogen and thyroid hormones) while others had not been associated with fear before (e.g., glucagon, ACTH). Additionally, several of these enriched metabolic receptors were coexpressed with well-described fear-modulating genes (Crh, Crhr1, or Crhr2). Co-expression analysis of monoamine markers and metabolic receptors suggested that monoaminergic nuclei have differential sensitivity to metabolic alterations. Serotonergic neurons expressed a large number of metabolic receptors (e.g., estrogen receptors, fatty acid receptors), suggesting a wide responsivity to metabolic changes. The noradrenergic system seemed to be specifically sensitive to hypocretin/orexin modulation. Taken together, we identified a number of novel metabolic factors (glucagon, ACTH) that have the potential to modulate the fear response. We additionally propose novel cerebral targets for metabolic factors (e.g., thyroid hormones) that modulate fear, but of which the sites of action are (largely) unknown

How metabolic state may regulate fear: Presence of metabolic receptors in the fear circuitry

Metabolic status impacts on the emotional brain to induce behavior that maintains energy balance. While hunger suppresses the fear circuitry to promote explorative food-seeking behavior, satiety or obesity may increase fear to prevent unnecessary risk-taking. Here we aimed to unravel which metabolic factors, that transfer information about the acute and the chronic metabolic status, are of primary importance to regulate fear, and to identify their sites of action within fear-related brain regions. We performed a de novo analysis of central and peripheral metabolic factors that can penetrate the blood-brain barrier using genome-wide expression data across the mouse brain from the Allen Brain Atlas (ABA). The central fear circuitry, as defined by subnuclei of the amygdala, the afferent hippocampus, the medial prefrontal cortex and the efferent periaqueductal gray, was enriched with metabolic receptors. Some of their corresponding ligands were known to modulate fear (e.g., estrogen and thyroid hormones) while others had not been associated with fear before (e.g., glucagon, ACTH). Additionally, several of these enriched metabolic receptors were coexpressed with well-described fear-modulating genes (Crh, Crhr1, or Crhr2). Co-expression analysis of monoamine markers and metabolic receptors suggested that monoaminergic nuclei have differential sensitivity to metabolic alterations. Serotonergic neurons expressed a large number of metabolic receptors (e.g., estrogen receptors, fatty acid receptors), suggesting a wide responsivity to metabolic changes. The noradrenergic system seemed to be specifically sensitive to hypocretin/orexin modulation. Taken together, we identified a number of novel metabolic factors (glucagon, ACTH) that have the potential to modulate the fear response. We additionally propose novel cerebral targets for metabolic factors (e.g., thyroid hormones) that modulate fear, but of which the sites of action are (largely) unknown.Pattern Recognition and Bioinformatic

Selective Glucocorticoid Receptor Modulation Prevents and Reverses Nonalcoholic Fatty Liver Disease in Male Mice

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