Anatomy of an ionized bubble at z=6.6: Which galaxies reionized the Universe?

Identifying the sources that drove cosmic reionization is a key goal of observational cosmology. Photons from these sources carved out ionized bubbles in the neutral intergalactic medium, and these bubbles gradually coalesced, resulting in a fully ionized Universe. The luminous z=6.6 'COLA1' galaxy lies in the epoch of reionization and shows a remarkable, double-peaked Lyman-alpha (Lya) line, the only one confirmed by multiple teams with high SNR and resolution. The detection of Lya flux bluewards of the systemic velocity means COLA1 resides in an ionized bubble. The exact velocity at which the blue Lya light is cut-off constrains the bubble size. This bubble provides a unique fortuitous, controlled environment -- since the bubble size is constrained, so is the total ionizing flux required to power it. Did COLA1 produce this ionizing flux all by itself? Or is it surrounded by large numbers of bright galaxies? Is a significant contribution from the faintest galaxies necessary? We propose to blindly identify emission-line galaxies within the ionized bubble and to obtain sensitive spectroscopy of COLA1 itself with slitless grism spectroscopy in the NIRCam F356W filter. The bubble size is well matched to the effective field of view for H-beta and the [OIII] doublet at z=6.6. We will obtain spectroscopic redshifts for all objects brighter than 0.1 L* (SFR>2 Msun/yr) and directly measure their ionizing photon production rate. We will then assess how much contribution from unseen galaxies is required. Through our detailed accounting of ionizing photons we will address the central question to reionization studies: was it bright or faint galaxies that reionized the universe

Where Cosmic Dawn Breaks First: Mapping the Primordial Overdensity Powering a z 9 Ionized Bubble

Models of cosmic reionization predict that the earliest star-forming systems develop in primordial overdensities which, in turn, create ionized bubbles. With time, these bubbles grow and coalesce until the intergalactic medium is fully ionized. Since Lyman-alpha photons originating in these protoclusters can propagate freely through ionized gas, the highest redshift Lyman Alpha emitters (LAEs) act as valuable tracers of early ionized bubbles. We present evidence that the highest redshift LAE, EGSz8p7 (z=8.68), is likely embedded in such an overdensity. Collectively, in all of HST's deep fields, blank fields and gravitationally-lensed fields spanning >1000 arcmin^2 there are ~30 photometric candidates at z~9, yet a third lie within 3.75' (10 cMpc) of EGSz8p7. To confirm and exploit this extraordinary early overdensity we seek systemic redshifts and diagnostic features only JWST can provide. We propose blind, grism spectroscopy to map the ionized bubble around EGSz8p7 using the [OIII] doublet. A blind survey is optimal for determining a complete census of EGSz8p7's physical neighbors. Spitzer/IRAC color excesses at z>8 imply extreme [OIII] EWs (~6000 A) ensuring efficient use of JWST. Stellar population modeling of the sources around EGSz8p7 may give us the strongest constraints yet on when star-formation first commenced after the Big Bang (i.e., cosmic dawn). Our spectra will likewise constrain the ionizing photon production efficiency, a key unknown in reionization calculations. Our observing strategy is designed for maximum legacy value with a footprint overlapping the CEERS ERS survey and use of the wide F444W grism that will guarantee additional

Azimuthal anisotropy of charged jet production in root s(NN)=2.76 TeV Pb-Pb collisions

We present measurements of the azimuthal dependence of charged jet production in central and semi-central root s(NN) = 2.76 TeV Pb-Pb collisions with respect to the second harmonic event plane, quantified as nu(ch)(2) (jet). Jet finding is performed employing the anti-k(T) algorithm with a resolution parameter R = 0.2 using charged tracks from the ALICE tracking system. The contribution of the azimuthal anisotropy of the underlying event is taken into account event-by-event. The remaining (statistical) region-to-region fluctuations are removed on an ensemble basis by unfolding the jet spectra for different event plane orientations independently. Significant non-zero nu(ch)(2) (jet) is observed in semi-central collisions (30-50% centrality) for 20 <p(T)(ch) (jet) <90 GeV/c. The azimuthal dependence of the charged jet production is similar to the dependence observed for jets comprising both charged and neutral fragments, and compatible with measurements of the nu(2) of single charged particles at high p(T). Good agreement between the data and predictions from JEWEL, an event generator simulating parton shower evolution in the presence of a dense QCD medium, is found in semi-central collisions. (C) 2015 CERN for the benefit of the ALICE Collaboration. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).Peer reviewe

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice