Galaxy And Mass Assembly (GAMA): Panchromatic Data Release (far-UV --- far-IR) and the low-z energy budget

We present the GAMA Panchromatic Data Release (PDR) constituting over 230deg$^2$ of imaging with photometry in 21 bands extending from the far-UV to the far-IR. These data complement our spectroscopic campaign of over 300k galaxies, and are compiled from observations with a variety of facilities including: GALEX, SDSS, VISTA, WISE, and Herschel, with the GAMA regions currently being surveyed by VST and scheduled for observations by ASKAP. These data are processed to a common astrometric solution, from which photometry is derived for 221,373 galaxies with r<19.8 mag. Online tools are provided to access and download data cutouts, or the full mosaics of the GAMA regions in each band. We focus, in particular, on the reduction and analysis of the VISTA VIKING data, and compare to earlier datasets (i.e., 2MASS and UKIDSS) before combining the data and examining its integrity. Having derived the 21-band photometric catalogue we proceed to fit the data using the energy balance code MAGPHYS. These measurements are then used to obtain the first fully empirical measurement of the 0.1-500$\mu$m energy output of the Universe. Exploring the Cosmic Spectral Energy Distribution (CSED) across three time-intervals (0.3-1.1Gyr, 1.1-1.8~Gyr and 1.8---2.4~Gyr), we find that the Universe is currently generating $(1.5 \pm 0.3) \times 10^{35}$ h$_{70}$ W Mpc$^{-3}$, down from $(2.5 \pm 0.2) \times 10^{35}$ h$_{70}$ W Mpc$^{-3}$ 2.3~Gyr ago. More importantly, we identify significant and smooth evolution in the integrated photon escape fraction at all wavelengths, with the UV escape fraction increasing from 27(18)% at z=0.18 in NUV(FUV) to 34(23)% at z=0.06. The GAMA PDR will allow for detailed studies of the energy production and outputs of individual systems, sub-populations, and representative galaxy samples at $z<0.5$. The GAMA PDR can be found at: http://gama-psi.icrar.org

Detailed Kinetics of the Direct Allo-Response in Human Liver Transplant Recipients: New Insights from an Optimized Assay

Conventional assays for quantification of allo-reactive T-cell precursor frequencies (PF) are relatively insensitive. We present a robust assay for quantification of PF of T-cells with direct donor-specificity, and establish the kinetics of circulating donor-specific T cells after liver transplantation (LTx). B cells from donor splenocytes were differentiated into professional antigen-presenting cells by CD40-engagement (CD40-B cells). CFSE-labelled PBMC from LTx-recipients obtained before and at several time points after LTx, were stimulated with donor-derived or 3rd party CD40-B cells. PF of donor-specific T cells were calculated from CFSE-dilution patterns, and intracellular IFN-γ was determined after re-stimulation with CD40-B cells. Compared to splenocytes, stimulations with CD40-B cells resulted in 3 to 5-fold higher responding T-cell PF. Memory and naïve T-cell subsets responded equally to allogeneic CD40-B cell stimulation. Donor-specific CD4+ and CD8+ T-cell PF ranged from 0.5 to 19% (median: 5.2%). One week after LTx, PF of circulating donor-specific CD4+ and CD8+ T cells increased significantly, while only a minor increase in numbers of T cells reacting to 3rd party allo-antigens was observed. One year after LTx numbers of CD4+ and CD8+ T cells reacting to donor antigens, as well as those reacting to 3rd party allo-antigens, were slightly lower compared to pre-transplant values. Moreover, CD4+ and CD8+ T cells responding to donor-derived, as well as those reacting to 3rd party CD40-B cells, produced less IFN-γ. In conclusion, our alternative approach enables detection of allo-reactive human T cells at high frequencies, and after application we conclude that donor-specific T-cell PF increase immediately after LTx. However, no evidence for a specific loss of circulating T-cells recognizing donor allo-antigens via the direct pathway up to 1 year after LTx was obtained, underscoring the relative insensitiveness of previous assays

Galaxy And Mass Assembly (GAMA): Panchromatic Data Release (far-UV-far-IR) and the low-z energy budget

This article has been accepted for publication in MNRAS ©: 2016: the authors. Published by Oxford University Press on behalf of the Royal Astronomical Society. All rights reserved.This work is supported by resources provided by the Pawsey Supercomputing Centre with funding from the Australian Government and the Government of Western Australi

TCR-mediated activation promotes GITR upregulation in T cells and resistance to glucocorticoid-induced death

C1 - Journal Articles RefereedT lymphocytes (pivotal in many inflammatory pathologies) are targets for glucocorticoid hormone (GC). How TCR-mediated activation and GC signaling via glucocorticoid receptor (GR) impact on T-cell fates is not fully defined. We delineated here the expression of a recently identified glucocorticoid-induced TNF receptor (GITR) induced by GC and by TCR-mediated T-cell activation in GC receptor (GR)-deficient mice (GR-/-). We also compared the action of GC on GITR+ and GITR- T cells by monitoring apoptosis, proliferation and cytokine production stimulated by anti-CD3 antibody. By using GR-/- mice, we observed that the development of GITR+ T cells (both in thymus and periphery) is not dependent upon GR signaling. This contradicts the implication of GITR's name reflecting GC induction. TCR-mediated T-cell activation induced GITR expression in both GR+/+ and GR-/- cells. Somewhat unexpectedly, there was very modest GITR upregulation on GR+/+ T cells by a range of GC doses (10(-8) to 10(-6) M). Constitutive expression of GITR by a subset of CD4+ cells did not significantly render them resistant to GC-induced cell death. However, TCR-induced GITR upregulation on GR+/+ T cells was correlated with resistance to GC-mediated apoptosis suggesting that GITR, in conjunction with other (as yet unidentified) TCR-induced factors, protects T cells from apoptosis. Thus, even though GC is a potent inducer of apoptosis of T cells, activated T cells are resistant to GC-mediated killing. Meanwhile, although GC suppressed anti-CD3-induced cytokine production, cell proliferation was unaffected by GC in GR+/+ mice. GR deficiency has no effect on anti-CD3-induced cytokine production and proliferation. Our findings also have implications for GC treatment in that it would be more difficult to abrogate an ongoing T-cell mediated inflammatory response than to prevent its induction

Monoclonal antibodies generated by DNA immunization recognize CD2 from a broad range of primates

© 2009 Australasian Society for Immunology Inc. All rights reserved.Using heterologous prime-boost (DNA immunization followed by immunization with transfected cells), we have generated depleting mouse anti-baboon CD2 monoclonal antibodies (mAb). These anti-CD2 mAb recognized a diverse range of primate CD2 from New World monkeys and Old World monkeys to humans and have potent immunosuppressive activity for human allo-MLR responses and anti-tetanus-toxoid recall responses. There was no upregulation of activation markers or release of cytokines when the mAb were incubated with human peripheral blood mononuclear cells. Using chimeric NOD-SCID IL2rγnull mice, the mAb were shown to deplete human and cynomolgus monkey T cells in vivo. These anti-CD2 mAb may therefore be important immunological tools in allo- and xenotransplantation.Jamie L. Brady, Stuart I. Mannering, Svjetlana Kireta, Patrick T. Coates, Anna I. Proietto, Peter J. Cowan, Anthony J. F. D'Apice and Andrew M. Le

Sleep problems and separation anxiety in preschool-aged children: A path analysis

Schlarb A, Jaeger S, Schneider S, In-Albon T, Hautzinger M. Sleep problems and separation anxiety in preschool-aged children: A path analysis. Journal of Child and Family Studies. 2016;25(3):902-910.Sleep problems occur frequently in young children, possibly causing detrimental effects on their development. Parental marital difficulties are known to put a burden on children’s sleep and adjustment. However, research concerning the relation between the parental relationship quality and children’s sleep difficulties is rare for preschool-aged children. This study aims to fill in the gap. Initially, caregivers of 94 preschoolers (41 girls and 53 boys, aged 2–6 years) filled in questionnaires providing information on their children’s sleep and anxiety as well as on their own sleep and relationship quality. A path model approach was used to examine two competing theoretical models linking these factors. The conducted path analysis indicated that children’s separation anxiety, β = −.134, p = .017, as well as their anxiety in general, β = −.177, p = .024, partially mediated the relation between the parental relationship quality and children’s sleep problems. Parental sleep problems correlated with the relationship quality, r = −.371, p = .030, but had no significant influence on children’s sleep. The results of our study suggest that children growing up with parents who state a low relationship quality might thus be concerned about the stability of their family system. As a result children’s sleep quality might be compromised due to irritation and feelings of insecurity. The study highlights the importance of the parental relationship as an influence factor in children’s sleep quality