Examining the Role of Environment in a Comprehensive Sample of Compact Groups

(Abridged) Compact groups, with their high number densities, small velocity dispersions, and an interstellar medium that has not been fully processed, provide a local analog to conditions of galaxy interactions in the earlier universe. The frequent and prolonged gravitational encounters that occur in compact groups affect the evolution of the constituent galaxies in a myriad of ways, for example gas processing and star formation. Recently, a statistically significant "gap" has been discovered mid-infrared IRAC colorspace of compact group galaxies. This gap is not seen in field samples and is a new example of how the compact group environment may affect the evolution of member galaxies. In order to investigate the origin and nature of this gap, we have compiled a sample of 49 compact groups. We find that a statistically significant deficit of galaxies in this gap region of IRAC colorspace is persistant in this sample, lending support to the hypothesis that the compact group environment inhibits moderate SSFRs. We note a curvature in the colorspace distribution, which is fully consistent with increasing dust temperature as the activity in a galaxy increases. This full sample of 49 compact groups allows us to subdivide the data according to physical properties of the groups. An analysis of these subsamples indicates that neither projected physical diameter nor density show a trend in colorspace within the values represented by this sample. We hypothesize that the apparent lack of a trend is due to the relatively small range of properties in this sample. Thus, the relative influence of stochastic effects becomes dominant. We analyze spectral energy distributions of member galaxies as a function of their location in colorspace and find that galaxies in different regions of MIR colorspace contain dust with varying temperatures and/or PAH emission.Comment: 24 pages, 13 figures. Accepted for publication in The Astronomical Journa

Some Like It Hot: Linking Diffuse X-ray Luminosity, Baryonic Mass, and Star Formation Rate in Compact Groups of Galaxies

We present an analysis of the diffuse X-ray emission in 19 compact groups of galaxies (CGs) observed with Chandra. The hottest, most X-ray luminous CGs agree well with the galaxy cluster X-ray scaling relations in $L_X-T$ and $L_X-\sigma$, even in CGs where the hot gas is associated with only the brightest galaxy. Using Spitzer photometry, we compute stellar masses and classify HCGs 19, 22, 40, and 42 and RSCGs 32, 44, and 86 as fossil groups using a new definition for fossil systems that includes a broader range of masses. We find that CGs with total stellar and HI masses $\gtrsim10^{11.3}$ M$_\odot$ are often X-ray luminous, while lower-mass CGs only sometimes exhibit faint, localized X-ray emission. Additionally, we compare the diffuse X-ray luminosity against both the total UV and 24 $\mu$m star formation rates of each CG and optical colors of the most massive galaxy in each of the CGs. The most X-ray luminous CGs have the lowest star formation rates, likely because there is no cold gas available for star formation, either because the majority of the baryons in these CGs are in stars or the X-ray halo, or due to gas stripping from the galaxies in CGs with hot halos. Finally, the optical colors that trace recent star formation histories of the most massive group galaxies do not correlate with the X-ray luminosities of the CGs, indicating that perhaps the current state of the X-ray halos is independent of the recent history of stellar mass assembly in the most massive galaxies.Comment: 20 pages, 7 figures, accepted for publication in Ap

The Mid-Infrared Instrument for the James Webb Space Telescope, VII: The MIRI Detectors

The MIRI Si:As IBC detector arrays extend the heritage technology from the Spitzer IRAC arrays to a 1024 x 1024 pixel format. We provide a short discussion of the principles of operation, design, and performance of the individual MIRI detectors, in support of a description of their operation in arrays provided in an accompanying paper (Ressler et al. (2015)). We then describe modeling of their response. We find that electron diffusion is an important component of their performance, although it was omitted in previous models. Our new model will let us optimize the bias voltage while avoiding avalanche gain. It also predicts the fraction of the IR-active layer that is depleted (and thus contributes to the quantum efficiency) as signal is accumulated on the array amplifier. Another set of models accurately predicts the nonlinearity of the detector-amplifier unit and has guided determination of the corrections for nonlinearity. Finally, we discuss how diffraction at the interpixel gaps and total internal reflection can produce the extended cross-like artifacts around images with these arrays at short wavelengths, ~ 5 microns. The modeling of the behavior of these devices is helping optimize how we operate them and also providing inputs to the development of the data pipeline

Maternal obesity has little effect on the immediate offspring but impacts on the next generation

Maternal obesity during pregnancy has been linked to an increased risk of obesity and cardiometabolic disease in the offspring, a phenomenon attributed to developmental programming. Programming effects may be transmissible across generations through both maternal and paternal inheritance, although the mechanisms remain unclear. Using a mouse model, we explored the effects of moderate maternal diet-induced obesity (DIO) on weight gain and glucose-insulin homeostasis in first-generation (F1) and second-generation offspring. DIO was associated with insulin resistance, hyperglycemia and dyslipidemia before pregnancy. Birth weight was reduced in female offspring of DIO mothers (by 6%, P = .039), and DIO offspring were heavier than controls at weaning (males by 47%, females by 27%), however there were no differences in glucose tolerance, plasma lipids, or hepatic gene expression at 6 months. Despite the relative lack of effects in the F1, we found clear fetal growth restriction and persistent metabolic changes in otherwise unmanipulated second-generation offspring with effects on birth weight, insulin levels, and hepatic gene expression that were transmitted through both maternal and paternal lines. This suggests that the consequences of the current dietary obesity epidemic may also have an impact on the descendants of obese individuals, even when the phenotype of the F1 appears largely unaffected

Extrinsic conditions influence the self-association and structure of IF1, the regulatory protein of mitochondrial ATP synthase.

The endogenous inhibitor of ATP synthase in mitochondria, called IF1, conserves cellular energy when the proton-motive force collapses by inhibiting ATP hydrolysis. Around neutrality, the 84-amino-acid bovine IF1 is thought to self-assemble into active dimers and, under alkaline conditions, into inactive tetramers and higher oligomers. Dimerization is mediated by formation of an antiparallel α-helical coiled-coil involving residues 44-84. The inhibitory region of each monomer from residues 1-46 is largely α-helical in crystals, but disordered in solution. The formation of the inhibited enzyme complex requires the hydrolysis of two ATP molecules, and in the complex the disordered region from residues 8-13 is extended and is followed by an α-helix from residues 14-18 and a longer α-helix from residue 21, which continues unbroken into the coiled-coil region. From residues 21-46, the long α-helix binds to other α-helices in the C-terminal region of predominantly one of the β-subunits in the most closed of the three catalytic interfaces. The definition of the factors that influence the self-association of IF1 is a key to understanding the regulation of its inhibitory properties. Therefore, we investigated the influence of pH and salt-types on the self-association of bovine IF1 and the folding of its unfolded region. We identified the equilibrium between dimers and tetramers as a potential central factor in the in vivo modulation of the inhibitory activity and suggest that the intrinsically disordered region makes its inhibitory potency exquisitely sensitive and responsive to physiological changes that influence the capability of mitochondria to make ATP

Characterising the Physiological Responses of Chinook Salmon (Oncorhynchus tshawytscha) Subjected to Heat and Oxygen Stress.

In New Zealand, during the hottest periods of the year, some salmon farms in the Marlborough Sounds reach water temperatures above the optimal range for Chinook salmon. High levels of mortality are recorded during these periods, emphasising the importance of understanding thermal stress in this species. In this study, the responses of Chinook salmon (Oncorhynchus tshawytscha) to chronic, long-term changes in temperature and dissolved oxygen were investigated. This is a unique investigation due to the duration of the stress events the fish were exposed to. Health and haematological parameters were analysed alongside gene expression results to determine the effects of thermal stress on Chinook salmon. Six copies of heat shock protein 90 (HSP90) were discovered and characterised: HSP90AA1.1a, HSP90AA1.2a, HSP90AA1.1b, HSP90AA1.2b, HSP90AB1a and HSP90AB1b, as well as two copies of SOD1, named SOD1a and SOD1b. The amino acid sequences contained features similar to those found in other vertebrate HSP90 and SOD1 sequences, and the phylogenetic tree and synteny analysis provided conclusive evidence of their relationship to other vertebrate HSP90 and SOD1 genes. Primers were designed for qPCR to enable the expression of all copies of HSP90 and SOD1 to be analysed. The expression studies showed that HSP90 and SOD1 were downregulated in the liver and spleen in response to longer term exposure to high temperatures and lower dissolved oxygen. HSP90 was also downregulated in the gill; however, the results for SOD1 expression in the gill were not conclusive. This study provides important insights into the physiological and genetic responses of Chinook salmon to temperature and oxygen stress, which are critical for developing sustainable fish aquaculture in an era of changing global climates

Short-term genome stability of serial Clostridium difficile ribotype 027 isolates in an experimental gut model and recurrent human disease

Copyright: © 2013 Eyre et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedClostridium difficile whole genome sequencing has the potential to identify related isolates, even among otherwise indistinguishable strains, but interpretation depends on understanding genomic variation within isolates and individuals.Serial isolates from two scenarios were whole genome sequenced. Firstly, 62 isolates from 29 timepoints from three in vitro gut models, inoculated with a NAP1/027 strain. Secondly, 122 isolates from 44 patients (2–8 samples/patient) with mostly recurrent/on-going symptomatic NAP-1/027 C. difficile infection. Reference-based mapping was used to identify single nucleotide variants (SNVs).Across three gut model inductions, two with antibiotic treatment, total 137 days, only two new SNVs became established. Pre-existing minority SNVs became dominant in two models. Several SNVs were detected, only present in the minority of colonies at one/two timepoints. The median (inter-quartile range) [range] time between patients’ first and last samples was 60 (29.5–118.5) [0–561] days. Within-patient C. difficile evolution was 0.45 SNVs/called genome/year (95%CI 0.00–1.28) and within-host diversity was 0.28 SNVs/called genome (0.05–0.53). 26/28 gut model and patient SNVs were non-synonymous, affecting a range of gene targets.The consistency of whole genome sequencing data from gut model C. difficile isolates, and the high stability of genomic sequences in isolates from patients, supports the use of whole genome sequencing in detailed transmission investigations.Peer reviewe

Protease-activated receptor 4 variant p.Tyr157Cys reduces platelet functional responses and alters receptor trafficking

OBJECTIVE—: Protease-activated receptor 4 (PAR4) is a key regulator of platelet reactivity and is encoded by F2RL3, which has abundant rare missense variants. We aimed to provide proof of principle that rare F2LR3 variants potentially affect on platelet reactivity and responsiveness to PAR1 antagonist drugs and to explore underlying molecular mechanisms. APPROACH AND RESULTS—: We identified 6 rare F2RL3 missense variants in 236 cardiac patients, of which the variant causing a tyrosine 157 to cysteine substitution (Y157C) was predicted computationally to affect most on PAR4 structure. Y157C platelets from 3 cases showed reduced responses to PAR4-activating peptide and to α-thrombin compared with controls, but no reduction in responses to PAR1-activating peptide. Pretreatment with the PAR1 antagonist vorapaxar caused lower residual α-thrombin responses in Y157C platelets than in controls, indicating greater platelet inhibition. HEK293 cells transfected with a PAR4 Y157C expression construct had reduced PAR4 functional responses, unchanged total PAR4 expression but reduced surface expression. PAR4 Y157C was partially retained in the endoplasmic reticulum and displayed an expression pattern consistent with defective N-glycosylation. Mutagenesis of Y322, which is the putative hydrogen bond partner of Y157, also reduced PAR4 surface expression in HEK293 cells. CONCLUSIONS—: Reduced PAR4 responses associated with Y157C result from aberrant anterograde surface receptor trafficking, in part, because of disrupted intramolecular hydrogen bonding. Characterization of PAR4 Y157C establishes that rare F2RL3 variants have the potential to markedly alter platelet PAR4 reactivity particularly after exposure to therapeutic PAR1 antagonists