Intensity Mapping with Carbon Monoxide Emission Lines and the Redshifted 21 cm Line

We quantify the prospects for using emission lines from rotational transitions of the CO molecule to perform an `intensity mapping' observation at high redshift during the Epoch of Reionization (EoR). The aim of CO intensity mapping is to observe the combined CO emission from many unresolved galaxies, to measure the spatial fluctuations in this emission, and use this as a tracer of large scale structure at very early times in the history of our Universe. This measurement would help determine the properties of molecular clouds -- the sites of star formation -- in the very galaxies that reionize the Universe. We further consider the possibility of cross-correlating CO intensity maps with future observations of the redshifted 21 cm line. The cross spectrum is less sensitive to foreground contamination than the auto power spectra, and can therefore help confirm the high redshift origin of each signal. Furthermore, the cross spectrum measurement would help extract key information about the EoR, especially regarding the size distribution of ionized regions. We discuss uncertainties in predicting the CO signal at high redshift, and discuss strategies for improving these predictions. Under favorable assumptions, and feasible specifications for a CO survey mapping the CO(2-1) and CO(1-0) lines, the power spectrum of CO emission fluctuations and its cross spectrum with future 21 cm measurements from the MWA are detectable at high significance.Comment: 19 pages, 8 figures, submitted to Ap

The Bolocam Galactic Plane Survey IX: Data Release 2 and Outer Galaxy Extension

We present a re-reduction and expansion of the Bolocam Galactic Plane Survey, first presented by Aguirre et al. (2011) and Rosolowsky et al. (2010). The BGPS is a 1.1 mm survey of dust emission in the Northern galactic plane, covering longitudes -10 < \ell < 90 and latitudes |b| < 0.5 with a typical 1-\sigma RMS sensitivity of 30-100 mJy in a 33" beam. Version 2 of the survey includes an additional 20 square degrees of coverage in the 3rd and 4th quadrants and 2 square degrees in the 1st quadrant. The new data release has improved angular recovery, with complete recovery out to 80" and partial recovery to 300", and reduced negative bowls around bright sources resulting from the atmospheric subtraction process. We resolve the factor of 1.5 flux calibration offset between the v1.0 data release and other data sets and determine that there is no offset between v2.0 and other data sets. The v2.0 pointing accuracy is tested against other surveys and demonstrated to be accurate and an improvement over v1.0. We present simulations and tests of the pipeline and its properties, including measurements of the pipeline's angular transfer function. The Bolocat cataloging tool was used to extract a new catalog, which includes 8594 sources, with 591 in the expanded regions. We have demonstrated that the Bolocat 40" and 80" apertures are accurate even in the presence of strong extended background emission. The number of sources is lower than in v1.0, but the amount of flux and area included in identified sources is larger.Comment: 36 pages, 16 figures, accepted to ApJS. Data available from http://irsa.ipac.caltech.edu/data/BOLOCAM_GPS

Galactic H2CO Densitometry I: Pilot survey of Ultracompact HII regions and methodology

We present a pilot survey of 21 lines of sight towards UCHII regions in the H2CO 1-1 (6cm) and 2-2 (2cm) transitions, using the H2CO centimeter lines as a molecular gas densitometer. Using Arecibo and Green Bank beam-matched observations, we measure the density of 51 detected H2CO line pairs and present upper limits on density for an additional 24 detected 1-1 lines. We analyze the systematic uncertainties in the H2CO densitometer, achieving H2 density measurements with accuracies ~ 0.1-0.3 dex. The densities measured are not correlated with distance, implying that it is possible to make accurate density measurements throughout the galaxy without a distance bias. We confirm that ultracompact HII regions are associated with gas at densities n(H2)~10^5cm^-3. The densities measured in line-of-sight molecular clouds suggest that they consist of low volume filling factor (f~10^-2) gas at high (n(H2)>10^4cm^-3) density, which is inconsistent with purely supersonic turbulence and requires high-density clumping greater than typically observed in gravoturbulent simulations. We observe complex line morphologies that indicate density variations with velocity around UCHII regions, and we classify a subset of the UCHII molecular envelopes as collapsing or expanding. We compare these measurements to Bolocam Galactic Plane Survey 1.1mm observations, and note that most UCHII regions have 1.1mm emission consisting of significant (5-70%) free-free emission and are therefore not necessarily dominated by optically thin dust emission. A comparison of our data with the Mangum et al. starburst sample shows that the area filling factor of dense (n(H2)~10^5cm^-3) molecular gas in typical starburst galaxies is <~0.01, but in extreme starburst galaxies like Arp 220, is ~0.1, suggesting that Arp 220 is physically similar to an oversized UCHII region.Comment: 39 pages, 46 figures, 8 tables, EmulateApJ 2-column format. Accepted for publication in ApJ. Full resolution version: http://casa.colorado.edu/~ginsbura/papers/h2co_pilot_draft0607.pdf, published at http://stacks.iop.org/0004-637X/736/14

Inhibition of Proliferation by PERK Regulates Mammary Acinar Morphogenesis and Tumor Formation

Endoplasmic reticulum (ER) stress signaling can be mediated by the ER kinase PERK, which phosphorylates its substrate eIF2α. This in turn, results in translational repression and the activation of downstream programs that can limit cell growth through cell cycle arrest and/or apoptosis. These responses can also be initiated by perturbations in cell adhesion. Thus, we hypothesized that adhesion-dependent regulation of PERK signaling might determine cell fate. We tested this hypothesis in a model of mammary acini development, a morphogenetic process regulated in part by adhesion signaling. Here we report a novel role for PERK in limiting MCF10A mammary epithelial cell proliferation during acinar morphogenesis in 3D Matrigel culture as well as in preventing mammary tumor formation in vivo. We show that loss of adhesion to a suitable substratum induces PERK-dependent phosphorylation of eIF2α and selective upregulation of ATF4 and GADD153. Further, inhibition of endogenous PERK signaling during acinar morphogenesis, using two dominant-negative PERK mutants (PERK-ΔC or PERK-K618A), does not affect apoptosis but results instead in hyper-proliferative and enlarged lumen-filled acini, devoid of proper architecture. This phenotype correlated with an adhesion-dependent increase in translation initiation, Ki67 staining and upregulation of Laminin-5, ErbB1 and ErbB2 expression. More importantly, the MCF10A cells expressing PERKΔC, but not a vector control, were tumorigenic in vivo upon orthotopic implantation in denuded mouse mammary fat pads. Our results reveal that the PERK pathway is responsive to adhesion-regulated signals and that it is essential for proper acinar morphogenesis and in preventing mammary tumor formation. The possibility that deficiencies in PERK signaling could lead to hyperproliferation of the mammary epithelium and increase the likelihood of tumor formation, is of significance to the understanding of breast cancer

Infection of human monocyte-derived dendritic cells by ANDES Hantavirus enhances pro-inflammatory state, the secretion of active MMP-9 and indirectly enhances endothelial permeability

<p>Abstract</p> <p>Background</p> <p>Andes virus (ANDV), a rodent-borne Hantavirus, is the major etiological agent of Hantavirus cardiopulmonary syndrome (HCPS) in South America, which is mainly characterized by a vascular leakage with high rate of fatal outcomes for infected patients. Currently, neither specific therapy nor vaccines are available against this pathogen. ANDV infects both dendritic and epithelial cells, but in despite that the severity of the disease directly correlates with the viral RNA load, considerable evidence suggests that immune mechanisms rather than direct viral cytopathology are responsible for plasma leakage in HCPS. Here, we assessed the possible effect of soluble factors, induced in viral-activated DCs, on endothelial permeability. Activated immune cells, including DC, secrete gelatinolytic matrix metalloproteases (gMMP-2 and -9) that modulate the vascular permeability for their trafficking.</p> <p>Methods</p> <p>A clinical ANDES isolate was used to infect DC derived from primary PBMC. Maturation and pro-inflammatory phenotypes of ANDES-infected DC were assessed by studying the expression of receptors, cytokines and active gMMP-9, as well as some of their functional status. The ANDES-infected DC supernatants were assessed for their capacity to enhance a monolayer endothelial permeability using primary human vascular endothelial cells (HUVEC).</p> <p>Results</p> <p>Here, we show that <it>in vitro </it>primary DCs infected by a clinical isolate of ANDV shed virus RNA and proteins, suggesting a competent viral replication in these cells. Moreover, this infection induces an enhanced expression of soluble pro-inflammatory factors, including TNF-α and the active gMMP-9, as well as a decreased expression of anti-inflammatory cytokines, such as IL-10 and TGF-β. These viral activated cells are less sensitive to apoptosis. Moreover, supernatants from ANDV-infected DCs were able to indirectly enhance the permeability of a monolayer of primary HUVEC.</p> <p>Conclusions</p> <p>Primary human DCs, that are primarily targeted by hantaviruses can productively be infected by ANDV and subsequently induce direct effects favoring a proinflammatory phenotype of infected DCs. Finally, based on our observations, we hypothesize that soluble factors secreted in ANDV-infected DC supernatants, importantly contribute to the endothelial permeability enhancement that characterize the HCPS.</p

Breeding habitat loss linked to declines in Rufous Hummingbirds

Habitat loss is the primary driver of biodiversity decline worldwide, but it remains unknown how land-cover change and, in general, habitat loss impact many migratory species, such as the Rufous Hummingbird (Selasphorus rufus). Here, we gathered 5115 occurrence records for the Rufous Hummingbird from professional and citizen-science data sets and parameterized species distribution models with four bioclimatic variables and two Landsat satellite spectral reflectance bands. We calculated the population change and change in the potential distribution of the Rufous Hummingbird across its breeding range in the Pacific Northwest of North America over the last 36 yr (1985–2021). Back-casting habitat suitability predictions over time, we provide the first quantifications of breeding habitat change for the Rufous Hummingbird, which has exhibited precipitous declines over the past two decades. Furthermore, we evaluated links between modeled habitat suitability, population abundance, and trends with a route-level analysis of Breeding Bird Survey data. We found notable habitat loss occurring in Bird Conservation Regions along the Pacific coast where the species is most abundant (54% and 34% decreases in suitable habitat area), with habitat loss in coastal regions linked to population decline. In contrast, we detected habitat gains in regions along the interior, northeastern edges of the breeding range (160% and 85% increases in suitable habitat area). However, increasing suitability does not guarantee species colonization of new habitat. Our results indicate the need to further investigate drivers of habitat loss, such as intensive forestry and suppression of early seral habitat, along the Pacific coast. Our modeling approach can be applied to efficiently detect and quantify habitat loss over time for a variety of taxa

Frequency of Ectodysplasin alleles and limited introgression between sympatric threespine stickleback populations. Environ

Abstract The threespine stickleback (Gasterosteus aculeatus) is primitively an anadromous or resident marine species but has repeatedly colonized fresh water, where predictable phenotypic divergence usually occurs rapidly. A conspicuous element of this divergence is change of the number and position of lateral armor plates from about 33 that cover the entire flank (complete) to &lt;10 anterior plates (low). This difference is caused primarily by variation at the Ectodysplasin (Eda) locus. The low Eda allele appears to be rarer in two geographically adjacent anadromous populations from Cook Inlet, Alaska than in most marine or anadromous populations reported from elsewhere, and there is no evidence of elevated gene flow for Eda between anadromous and resident lake threespine stickleback populations that breed in sympatry. However, the two anadromous populations are divergent for the frequencies of two complete Eda alleles. It is not clear how monomorphic low-plated freshwater populations in Cook Inlet have almost invariably acquired ancestral low Eda alleles from anadromous ancestors in which this allele appears to be extremely rare