The Role of Star Formation and an AGN in Dust Heating of z = 0.3–2.8 Galaxies. I. Evolution with Redshift and Luminosity

We characterize infrared spectral energy distributions of 343 (ultra)luminous infrared galaxies from z = 0.3–2.8. We diagnose the presence of an active galactic nucleus (AGN) by decomposing individual Spitzer mid-IR spectroscopy into emission from star formation and an AGN-powered continuum; we classify sources as star-forming galaxies (SFGs), AGNs, or composites. Composites comprise 30% of our sample and are prevalent at faint and bright S_(24), making them an important source of IR AGN emission. We combine spectroscopy with multiwavelength photometry, including Herschel imaging, to create three libraries of publicly available templates (2–1000 μm). We fit the far-IR emission using a two-temperature modified blackbody to measure cold and warm dust temperatures (T_c and T_w). We find that T_c does not depend on mid-IR classification, while T_w shows a notable increase as the AGN grows more luminous. We measure a quadratic relationship between mid-IR AGN emission and total AGN contribution to LIR. AGNs, composites, and SFGs separate in S_8/S_(3.6) and S_(250)/S_(24), providing a useful diagnostic for estimating relative amounts of these sources. We estimate that >40% of IR-selected samples host an AGN, even at faint selection thresholds (S_(24) > 100 μJy). Our decomposition technique and color diagnostics are relevant given upcoming observations with the James Webb Space Telescope

A controlled study of cold dust content in galaxies from z=0−2z=0-2

At $z=1-3$, the formation of new stars is dominated by dusty galaxies whose far-IR emission indicates they contain colder dust than local galaxies of a similar luminosity. We explore the reasons for the evolving IR emission of similar galaxies over cosmic time using: 1) Local galaxies from GOALS $(L_{\rm IR}=10^{11}-10^{12}\,L_\odot)$; 2) Galaxies at $z\sim0.1-0.5$ from the 5MUSES ($L_{\rm IR}=10^{10}-10^{12}\,L_\odot$); 3) IR luminous galaxies spanning $z=0.5-3$ from GOODS and Spitzer xFLS ($L_{\rm IR}>10^{11}\,L_\odot$). All samples have Spitzer mid-IR spectra, and Herschel and ground-based submillimeter imaging covering the full IR spectral energy distribution, allowing us to robustly measure $L_{\rm IR}^{\rm\scriptscriptstyle SF}$, $T_{\rm dust}$, and $M_{\rm dust}$ for every galaxy. Despite similar infrared luminosities, $z>0.5$ dusty star forming galaxies have a factor of 5 higher dust masses and 5K colder temperatures. The increase in dust mass is linked with an increase in the gas fractions with redshift, and we do not observe a similar increase in stellar mass or star formation efficiency. $L_{160}^{\rm\scriptscriptstyle SF}/L_{70}^{\rm\scriptscriptstyle SF}$, a proxy for $T_{\rm dust}$, is strongly correlated with $L_{\rm IR}^{\rm\scriptscriptstyle SF}/M_{\rm dust}$ independently of redshift. We measure merger classification and galaxy size for a subsample, and there is no obvious correlation between these parameters and $L_{\rm IR}^{\rm \scriptscriptstyle SF}/M_{\rm dust}$ or $L_{160}^{\rm\scriptscriptstyle SF}/L_{70}^{\rm\scriptscriptstyle SF}$. In dusty star forming galaxies, the change in $L_{\rm IR}^{\rm\scriptscriptstyle SF}/M_{\rm dust}$ can fully account for the observed colder dust temperatures, suggesting that any change in the spatial extent of the interstellar medium is a second order effect.Comment: Accepted for publication in ApJ. 21 pages, 11 figure

Interaction of ARC and Daxx: a novel endogenous target to preserve motor function and cell loss after focal brain ischemia in mice

The aim of this study was to explore the signaling and neuroprotective effect of transactivator of transcription (TAT) protein transduction of the apoptosis repressor with CARD (ARC) in in vitro and in vivo models of cerebral ischemia in mice. In mice, transient focal cerebral ischemia reduced endogenousARCprotein in neurons in the ischemic striatum at early reperfusion time points, and in primary neuronal cultures, RNA interference resulted in greater neuronal susceptibility to oxygen glucose deprivation (OGD).TAT.ARC protein delivery led to a dose-dependent better survival after OGD. Infarct sizes 72 h after 60 min middle cerebral artery occlusion (MCAo) were on average 30±8% (mean±SD; p=0.005; T2-weighted MRI) smaller in TAT.ARC-treated mice (1ug intraventricularly during MCAo) compared with controls. TAT.ARC-treated mice showed better performance in the pole test compared with TAT.β-Gal-treated controls. Importantly, post-stroke treatment (3 h after MCAo) was still effective in affording reduced lesion volume by 20±7% (mean±SD; p˃0.05) and better functional outcome compared with controls. Delayed treatment in mice subjected to 30 min MCAo led to sustained neuroprotection and functional behavior benefits for at least 28 d. Functionally, TAT.ARC treatment inhibited DAXX–ASK1–JNK signaling in the ischemic brain. ARC interacts with DAXX in a CARD-dependent manner to block DAXX trafficking and ASK1–JNK activation. Our work identifies for the first time ARC–DAXX binding to block ASK1–JNK activation as an ARC-specific endogenous mechanism that interferes with neuronal cell death and ischemic brain injury. Delayed delivery of TAT.ARC may present a promising target for stroke therapy

Re-visiting the extended Schmidt law: the important role of existing stars in regulating star formation

We revisit the proposed extended Schmidt law (Shi et al. 2011) which points that the star formation efficiency in galaxies depends on the stellar mass surface density, by investigating spatially-resolved star formation rates (SFRs), gas masses and stellar masses of star formation regions in a vast range of galactic environments, from the outer disks of dwarf galaxies to spiral disks and to merging galaxies as well as individual molecular clouds in M33. We find that these regions are distributed in a tight power-law as Sigma_SFR ~(Sigma_star^0.5 Sigma_gas )^1.09, which is also valid for the integrated measurements of disk and merging galaxies at high-z. Interestingly, we show that star formation regions in the outer disks of dwarf galaxies with Sigma_SFR down to 10^(-5) Msun/yr/kpc^2, which are outliers of both Kennicutt-Schmidt and Silk-Elmegreen law, also follow the extended Schmidt law. Other outliers in the Kennicutt-Schmidt law, such as extremely-metal poor star-formation regions, also show significantly reduced deviations from the extended Schmidt law. These results suggest an important role for existing stars in helping to regulate star formation through the effect of their gravity on the mid-plane pressure in a wide range of galactic environments.Comment: 15 pages, 6 figures, 3 tables; ApJ in pres

Easy-Processable and Aging-Free All-Polymer Polysiloxane Composites

Here, we report all-polymer polysiloxane composites that overcome the long-standing processing problems of silica-reinforced silicone rubbers. Polystyrene fillers are dispersed with styrene/dimethylsiloxane symmetric diblock and triblock copolymers that control the filler morphology, filler–matrix interactions, and filler–filler interactions. Surprisingly, the composites not only rival the traditional silica-reinforced polysiloxane in mechanical properties of cured materials but also have better processability and stability than the silica-filled compound before curing. Large amplitude oscillatory shear experiments demonstrate that the triblock copolymer addition strongly affects the rheological properties. We hypothesize that the bridges and entangled loops that were formed by the triblock copolymer can connect different PS domains to provide additional reinforcement. The aging effect that originates from PDMS chain adsorption on the filler particle surface is also avoided because of the thermodynamic repulsion between PS and PDMS phases

Extended Schmidt Law: Role Of Existing Stars In Current Star Formation

We propose an "extended Schmidt law" with explicit dependence of the star formation efficiency (SFE=SFR/Mgas) on the stellar mass surface density. This relation has a power-law index of 0.48+-0.04 and an 1-sigma observed scatter on the SFE of 0.4 dex, which holds over 5 orders of magnitude in the stellar density for individual global galaxies including various types especially the low-surface-brightness (LSB) galaxies that deviate significantly from the Kennicutt-Schmidt law. When applying it to regions at sub-kpc resolution of a sample of 12 spiral galaxies, the extended Schmidt law not only holds for LSB regions but also shows significantly smaller scatters both within and across galaxies compared to the Kennicutt-Schmidt law. We argue that this new relation points to the role of existing stars in regulating the SFE, thus encoding better the star formation physics. Comparison with physical models of star formation recipes shows that the extended Schmidt law can be reproduced by some models including gas free-fall in a stellar-gravitational potential and pressure-supported star formation. By implementing this new law into the analytic model of gas accretion in Lambda CDM, we show that it can re-produce the observed main sequence of star-forming galaxies (a relation between the SFR and stellar mass) from z=0 up to z=2.Comment: 18 pages, 9 figures; Accepted for Publication In Ap

CTD kinase I is required for the integrity of the rDNA tandem array

The genomic stability of the rDNA tandem array is tightly controlled to allow sequence homogenization and to prevent deleterious rearrangements. In this report, we show that the absence of the yeast CTD kinase I (CTDK-I) complex in null mutant strains leads to a decrease in the number of tandem rDNA repeats. Reintroduction of the missing gene induces an increase of rDNA repeats to reach a copy number similar to that of the original strain. Interestingly, while expansion is dependent on Fob1, a protein required for replication fork blocking activity in rDNA, contraction occurs in the absence of Fob1. Furthermore, silencing of class II genes at the rDNA, a process connected to rDNA stability, is not affected. Ctk1, the kinase subunit of the CTDK-I complex is involved in various steps of mRNA synthesis. In addition, we have recently shown that Ctk1 is also implicated in rRNA synthesis. The results suggest that the RNA polymerase I transcription defect occurring in a ctk1 mutant strain causes rDNA contraction

Successful Expansion but Not Complete Restriction of Tropism of Adeno-Associated Virus by In Vivo Biopanning of Random Virus Display Peptide Libraries

Targeting viral vectors to certain tissues in vivo has been a major challenge in gene therapy. Cell type-directed vector capsids can be selected from random peptide libraries displayed on viral capsids in vitro but so far this system could not easily be translated to in vivo applications. Using a novel, PCR-based amplification protocol for peptide libraries displayed on adeno-associated virus (AAV), we selected vectors for optimized transduction of primary tumor cells in vitro. However, these vectors were not suitable for transduction of the same target cells under in vivo conditions. We therefore performed selections of AAV peptide libraries in vivo in living animals after intravenous administration using tumor and lung tissue as prototype targets. Analysis of peptide sequences of AAV clones after several rounds of selection yielded distinct sequence motifs for both tissues. The selected clones indeed conferred gene expression in the target tissue while gene expression was undetectable in animals injected with control vectors. However, all of the vectors selected for tumor transduction also transduced heart tissue and the vectors selected for lung transduction also transduced a number of other tissues, particularly and invariably the heart. This suggests that modification of the heparin binding motif by target-binding peptide insertion is necessary but not sufficient to achieve tissue-specific transgene expression. While the approach presented here does not yield vectors whose expression is confined to one target tissue, it is a useful tool for in vivo tissue transduction when expression in tissues other than the primary target is uncritical

Antimicrobial resistance among migrants in Europe: a systematic review and meta-analysis

BACKGROUND: Rates of antimicrobial resistance (AMR) are rising globally and there is concern that increased migration is contributing to the burden of antibiotic resistance in Europe. However, the effect of migration on the burden of AMR in Europe has not yet been comprehensively examined. Therefore, we did a systematic review and meta-analysis to identify and synthesise data for AMR carriage or infection in migrants to Europe to examine differences in patterns of AMR across migrant groups and in different settings. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, Embase, PubMed, and Scopus with no language restrictions from Jan 1, 2000, to Jan 18, 2017, for primary data from observational studies reporting antibacterial resistance in common bacterial pathogens among migrants to 21 European Union-15 and European Economic Area countries. To be eligible for inclusion, studies had to report data on carriage or infection with laboratory-confirmed antibiotic-resistant organisms in migrant populations. We extracted data from eligible studies and assessed quality using piloted, standardised forms. We did not examine drug resistance in tuberculosis and excluded articles solely reporting on this parameter. We also excluded articles in which migrant status was determined by ethnicity, country of birth of participants' parents, or was not defined, and articles in which data were not disaggregated by migrant status. Outcomes were carriage of or infection with antibiotic-resistant organisms. We used random-effects models to calculate the pooled prevalence of each outcome. The study protocol is registered with PROSPERO, number CRD42016043681. FINDINGS: We identified 2274 articles, of which 23 observational studies reporting on antibiotic resistance in 2319 migrants were included. The pooled prevalence of any AMR carriage or AMR infection in migrants was 25·4% (95% CI 19·1-31·8; I2 =98%), including meticillin-resistant Staphylococcus aureus (7·8%, 4·8-10·7; I2 =92%) and antibiotic-resistant Gram-negative bacteria (27·2%, 17·6-36·8; I2 =94%). The pooled prevalence of any AMR carriage or infection was higher in refugees and asylum seekers (33·0%, 18·3-47·6; I2 =98%) than in other migrant groups (6·6%, 1·8-11·3; I2 =92%). The pooled prevalence of antibiotic-resistant organisms was slightly higher in high-migrant community settings (33·1%, 11·1-55·1; I2 =96%) than in migrants in hospitals (24·3%, 16·1-32·6; I2 =98%). We did not find evidence of high rates of transmission of AMR from migrant to host populations. INTERPRETATION: Migrants are exposed to conditions favouring the emergence of drug resistance during transit and in host countries in Europe. Increased antibiotic resistance among refugees and asylum seekers and in high-migrant community settings (such as refugee camps and detention facilities) highlights the need for improved living conditions, access to health care, and initiatives to facilitate detection of and appropriate high-quality treatment for antibiotic-resistant infections during transit and in host countries. Protocols for the prevention and control of infection and for antibiotic surveillance need to be integrated in all aspects of health care, which should be accessible for all migrant groups, and should target determinants of AMR before, during, and after migration. FUNDING: UK National Institute for Health Research Imperial Biomedical Research Centre, Imperial College Healthcare Charity, the Wellcome Trust, and UK National Institute for Health Research Health Protection Research Unit in Healthcare-associated Infections and Antimictobial Resistance at Imperial College London

Unraveling gene regulatory networks from time-resolved gene expression data -- a measures comparison study

Peer reviewedPublisher PD