| 1. |
- Cirasuolo, M., et al.
(författare)
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MOONS: the Multi-Object Optical and Near-infrared Spectrograph for the VLT
- 2014
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Ingår i: Ground-based and Airborne Instrumentation for Astronomy V. - : SPIE. - 1996-756X .- 0277-786X. ; 9147, s. 91470-91470
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Konferensbidrag (refereegranskat)abstract
- MOONS (the Multi-Object Optical and Near-infrared Spectrograph) has been selected by ESO as a third-generation instrument for the Very Large Telescope (VLT). The light grasp of the large collecting area offered by the VLT (8.2m diameter), combined with the large multiplex and wavelength coverage (optical to near-IR: 0.8 -1.8 mu m) of MOONS will provide the European astronomical community with a powerful, unique instrument able to pioneer a wide range of Galactic, extragalactic and cosmological studies, and it will provide crucial follow-up for major facilities such as Gaia, VISTA, Euclid and LSST. MOONS has the observational power needed to unveil galaxy formation and evolution over the entire history of the Universe, from stars in our Milky Way, through the redshift desert, and up to the epoch of very first galaxies and reionization of the Universe at redshifts of z > 8-9, just a few million years after the Big Bang. From five years of observations MOONS will provide high-quality spectra for > 3M stars in our Galaxy and the Local Group, and for 1-2M galaxies at z > 1 (for an SDSS-like survey), promising to revolutionize our understanding of the Universe. The baseline design consists of similar to 1000 fibres, deployable over a field-of-view of similar to 500 arcmin(2), the largest patrol field offered by the Nasmyth focus at the VLT. The total wavelength coverage is 0.8 -1.8 mu m with two spectral resolving powers: in the medium-resolution mode (R similar to 4,000-6,000) the entire wavelength range is observed simultaneously, while the high-resolution mode will cover three selected sub-regions simultaneously: one region with R similar to 8,000 near the Ca II triplet to measure stellar radial velocities, and two regions at R similar to 20,000 (one in each of the J- and H-bands), for precision measurements of chemical abundances.
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| 2. |
- Koprowski, M. P., et al.
(författare)
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A direct calibration of thtae IRX-β relation in Lyman-break Galaxies at z = 3-5
- 2018
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Ingår i: Monthly Notices of the Royal Astronomical Society. - : Oxford University Press (OUP). - 0035-8711 .- 1365-2966. ; 479:4, s. 4355-4366
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Tidskriftsartikel (refereegranskat)abstract
- We use a sample of 4209 Lyman-break galaxies (LBGs) at z ≃ 3, 4, and 5 in the UKIRT Infrared Deep Sky Survey Ultra Deep Survey field to investigate the relationship between the observed slope of the stellar continuum emission in the ultraviolet, β, and the thermal dust emission, as quantified via the so-called 'infrared excess' (IRX=LIR/LUV). Through a stacking analysis, we directly measure the 850-μm flux density of LBGs in our deep (0.9 mJy) James Clerk Maxwell Telescope SCUBA-2 850-μm map as well as deep public Herschel/SPIRE 250-, 350-, and 500-μm imaging. We establish functional forms for the IRX-β relation to z ~ 5, confirming that there is no significant redshift evolution of the relation, and that the resulting average IRX-β curve is consistent with a Calzetti-like attenuation law. Comparing our results with recent works in the literature, we confirm that discrepancies in the slope of the IRX-β relation are driven by biases in the methodology used to determine the ultraviolet slopes. Consistent results are found when IRX-β is evaluated by stacking in bins of stellar mass, and we argue that the near-linear IRX-M* relationship is a better proxy for correcting observed ultraviolet luminosities to total star formation rates, provided an accurate handle on M* and also gives clues as to the physical driver of the role of dust-obscured star formation in high-redshift galaxies.
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| 3. |
- Bhadury, Joydeep, et al.
(författare)
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BET and HDAC inhibitors induce similar genes and biological effects and synergize to kill in Myc-induced murine lymphoma
- 2014
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 111:26
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Tidskriftsartikel (refereegranskat)abstract
- The bromodomain and extraterminal (BET) domain family of proteins binds to acetylated lysines on histones and regulates gene transcription. Recently, BET inhibitors (BETi) have been developed that show promise as potent anticancer drugs against various solid and hematological malignancies. Here we show that the structurally novel and orally bioavailable BET inhibitor RVX2135 inhibits proliferation and induces apoptosis of lymphoma cells arising in Myc-transgenic mice in vitro and in vivo. We find that BET inhibition exhibits broad transcriptional effects in Myc-transgenic lymphoma cells affecting many transcription factor networks. By examining the genes induced by BETi, which have largely been ignored to date, we discovered that these were similar to those induced by histone deacetylase inhibitors (HDACi). HDACi also induced cell-cycle arrest and cell death of Myc-induced murine lymphoma cells and synergized with BETi. Our data suggest that BETi sensitize Myc-overexpressing lymphoma cells partly by inducing HDAC-silenced genes, and suggest synergistic and therapeutic combinations by targeting the genetic link between BETi and HDACi.
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| 4. |
- Muralidharan, Somsundar Veppil, et al.
(författare)
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BET bromodomain inhibitors synergize with ATR inhibitors to induce DNA damage, apoptosis, senescence-associated secretory pathway and ER stress in Myc-induced lymphoma cells.
- 2016
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Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 1476-5594 .- 0950-9232. ; 35, s. 4689-4697
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Tidskriftsartikel (refereegranskat)abstract
- Inhibiting the bromodomain and extra-terminal (BET) domain family of epigenetic reader proteins has been shown to have potent anti-tumoral activity, which is commonly attributed to suppression of transcription. In this study, we show that two structurally distinct BET inhibitors (BETi) interfere with replication and cell cycle progression of murine Myc-induced lymphoma cells at sub-lethal concentrations when the transcriptome remains largely unaltered. This inhibition of replication coincides with a DNA-damage response and enhanced sensitivity to inhibitors of the upstream replication stress sensor ATR in vitro and in mouse models of B-cell lymphoma. Mechanistically, ATR and BETi combination therapy cause robust transcriptional changes of genes involved in cell death, senescence-associated secretory pathway, NFkB signaling and ER stress. Our data reveal that BETi can potentiate the cell stress and death caused by ATR inhibitors. This suggests that ATRi can be used in combination therapies of lymphomas without the use of genotoxic drugs.Oncogene advance online publication, 25 January 2016; doi:10.1038/onc.2015.521.
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