Near-infrared imaging of 222 nearby Hdelta-strong galaxies from the SDSS

We present UFTI K-band imaging observations of 222 galaxies that are selected from the Sloan Digital Sky Survey to have unusually strong Hdelta absorption equivalent widths, W(Hd)>4A. Using GIM2D, the images are fit with two-dimensional surface brightness models consisting of a simple disk and bulge component to derive B/T, the fraction of luminosity in the bulge. We find that the galaxies with weak or absent Halpha or [OII] emission (known as k+a galaxies) are predominantly bulge-dominated (with a mode of B/T~0.6), while galaxies with nebular emission (known as e[a] galaxies) are mostly disk-dominated (B/T~0.1). The morphologies and (r-k) colours of most k+a galaxies are inconsistent with the hypothesis that they result from the truncation of star formation in normal, spiral galaxies. However, their (u-g) and (r-k) colours, as well as their Hdelta line strengths, form a sequence that is well matched by a model in which >5 per cent of the stellar mass has been produced in a recent starburst. The lack of scatter in the dust-sensitive (r-k) colours suggests that the unusual spectra of k+a galaxies are not due to the effects of dust. The e(a) galaxies, on the other hand, have a colour distribution that is distinct from the k+a population, and typical of normal or dusty (tauV~2) spiral galaxies. We conclude that many e(a) galaxies are not progenitors of k+a galaxies, but are a separate phenomenon. Both k+a and e(a) galaxies reside in environments (characterized by the local density of galaxies brighter than Mr=-20) that are typical of normal galaxies and that are inconsistent with overdense regions like rich galaxy clusters.Comment: MNRAS, in press. 18 pages in mn2e style, with 10 inline figures and two long tables. Appendix figures provided as separate, low resolution gif images. Full paper with inline figures available at http://quixote.uwaterloo.ca/~mbalogh/papers/EA.ps.g

NEPSC2, the North Ecliptic Pole SCUBA-2 survey: 850-<i>μ</i>m map and catalogue of 850-<i>μ</i>m selected sources over 2 deg²

Abstract We present an 850-μm mosaic map and extracted catalogue of submillimetre sources in the extended North Ecliptic Pole (NEP) region over about 2 deg2. The 850-μm map is constructed using newly obtained observations by SCUBA-2 at the East Asian Observatory’s James Clerk Maxwell Telescope, carried out using the observatory’s large programme opportunities. The recent 850-μm survey has extended the submillimetre data coverage by almost a factor of 4 compared to previous surveys, with a depth of σrms = 1.0–2.3 mJy beam−1. The catalogue contains 549 sources selected above a significance level of 4σ, where the false-detection rate is 10 per cent; a higher threshold of 4.5σ is required in order to achieve a false-detection rate below 3 per cent, which results in 342 sources being selected. Despite the large spatial variation of the noise, the deboosted flux density of sources is comparable to results from the SCUBA-2 Cosmology Legacy Survey (S2CLS), which covered the central 0.6 deg2 of our survey area with better sensitivity. We construct the source counts at 850 μm, finding results in agreement with other 850-μm surveys in cosmological blank fields over S850 = 4–15 mJy. We find a slight excess of bright galaxies (S850 > 15 mJy), which can be considered to be at ɀphot = 2–4. The 850-μm data adds valuable long-wavelength information to mid-infrared-selected sources from the AKARI NEP-deep and NEP-wide surveys, which will be helpful in preparing for future near-infrared to millimetre wavelength observations in the NEP region. Our 850-μm mosaic map and source catalogue will be made publicly available

A multi-targeted approach to suppress tumor-promoting inflammation

Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-κB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes

A tale of two feedbacks: star formation in the host galaxies of radio AGNs

Several lines of argument support the existence of a link between activity at the nuclei of galaxies, in the form of an accreting supermassive black hole, and star formation activity in these galaxies. Radio jets have long been argued to be an ideal mechanism that allows active galactic nuclei (AGNs) to interact with their host galaxies and affect star formation. We use a sample of radio sources in the North Ecliptic Pole (NEP) field to study the nature of this putative link, by means of spectral energy distribution (SED) fitting. We employ the excellent spectral coverage of the AKARI infrared space telescope and the rich ancillary data available in the NEP to build SEDs extending from UV to far-IR wavelengths. We find a significant AGN component in our sample of relatively faint radio sources (<mJy). A positive correlation is found between the luminosity of the AGN component and that of star formation in the host galaxy, independent of the radio luminosity. In contrast, for narrow redshift and AGN luminosity ranges, we find that increasing radio luminosity leads to a decrease in the specific star formation rate. The most radio-loud AGNs are found to lie on the main sequence of star formation for their respective redshifts. For the first time, we potentially see such a two-sided feedback process in the same sample. We discuss the possible suppression of star formation, but not total quenching, in systems with strong radio jets, that supports the maintenance nature of feedback from radio AGN jets

CNVs in Three Psychiatric Disorders

BACKGROUND: We aimed to determine the similarities and differences in the roles of genic and regulatory copy number variations (CNVs) in bipolar disorder (BD), schizophrenia (SCZ), and autism spectrum disorder (ASD). METHODS: Based on high-resolution CNV data from 8708 Japanese samples, we performed to our knowledge the largest cross-disorder analysis of genic and regulatory CNVs in BD, SCZ, and ASD. RESULTS: In genic CNVs, we found an increased burden of smaller (500 kb) exonic CNVs in SCZ/ASD. Pathogenic CNVs linked to neurodevelopmental disorders were significantly associated with the risk for each disorder, but BD and SCZ/ASD differed in terms of the effect size (smaller in BD) and subtype distribution of CNVs linked to neurodevelopmental disorders. We identified 3 synaptic genes (DLG2, PCDH15, and ASTN2) as risk factors for BD. Whereas gene set analysis showed that BD-associated pathways were restricted to chromatin biology, SCZ and ASD involved more extensive and similar pathways. Nevertheless, a correlation analysis of gene set results indicated weak but significant pathway similarities between BD and SCZ or ASD (r = 0.25–0.31). In SCZ and ASD, but not BD, CNVs were significantly enriched in enhancers and promoters in brain tissue. CONCLUSIONS: BD and SCZ/ASD differ in terms of CNV burden, characteristics of CNVs linked to neurodevelopmental disorders, and regulatory CNVs. On the other hand, they have shared molecular mechanisms, including chromatin biology. The BD risk genes identified here could provide insight into the pathogenesis of BD