45 research outputs found

    Collage Vol. II

    Get PDF
    JUDY COCHRAN: Editorial, 4-5 ROBERTA CHAPMEN: Photo, 6 ANITRA CHUGHTAI (Translations): Haikus, 7 CHARLES O\u27KEEFE: Photo, 8 MARK VANDERLINDE-ABERNATHY, ALYSSA LANDRY (Translator): Memories of a Spider (Les souvenirs d\u27une araignee), 9 MARK VANDERLINE-ABERNATHY, AMY NORSKOG (Translator): Tomato Fields (Champ de tomates), 10 SARAH BISHOP, HEFEDH ZANINA (Translator): Dear John (Cher John), 11 RYAN BUTZ (Translator): Basho\u27s Haiku, Issa\u27s Haiku, 12-13 JENNIFER HUMBERT, FADOUA EL BOUAMRAOUI (Translator): Pressed Lips (Levres Serrees), 15 ADELE REEVES (Translator): Contemporary song by Mr. Children, 16-17 BRODY PAGEL, GRACE DUGAR (Translator): The Lizard King (Le Roi Lezard), 18 JIMMY PIPKIN (Translator): In Love with You, 19 MOLLY ROSCOE: Saturday Night at Rusty\u27s (Samedi Soir a Rusty\u27s), 20 CHARLES O\u27KEEFE: Photo, 21 MATT MESSMER (Translator): Waseda University School Song, 22-23 TIMOTHY COOPER: Wenn du grosh bist… (When you\u27re Tall…), 24 DAVID HARMAN: Der Dunkle Stern (The Dark Star), 25 ANN TOWNSEND, JUDY COCHRAN (Translator): From a Window (D\u27une Fenetre), 26-27 SARA CAHILL: El sauce lloron (The Weeping Willow), 28-32 CHARLES O\u27KEEFE: Photo, 30 JENNIFER HUMBERT, MATT BISHOP: Past, Present (passe, present), 33 CAROL GENEYA KAPLAN, FADOUA EL BOUAMRAOUI (Translator): Une Autre Femme (Another Woman), 34-35 CHARLES O\u27KEEFE: Photo, 36 ANN TOWNSEND, JUDY COCHRAN (Translator): The Mowers (Les Faucheurs), 37 PRISCILLA PATON: Photo, 38 GONZALO TUESTA: La Grande Dame De Paris (The Great Lady of Paris), 39 SARAH PILLERDORF (Translator): Japanese Cartoons by Tezuka Osamu, 41-45 DANIELLE GERKEN: Schuhe der Heimat (Boots of Home), 47 CURTIS PLOWGIAN: Le peste de la langue francaise, 48-52 PRISCILLA PATON: Photo, 50 ZANE HOUSEHOLDER: Vive la Republique! (Film), 54 JENNIFER ZIMMER: EL tenis y las frustraciones (Tennis and Frustrations), La tumba de Ben (Ben\u27s Grave), 56-57 AUTUMN LOTZE: Times Square in the rain, 58-59 CHARLES O\u27KEEFE: Photo, 60 STEPHEN M. JULKA: Colors of the Earth, 61 THOMAS BRESSOUD: Java, 62 ERIC NELSON: World, 63 SARAH CLAPP (Translator): At a long day\u27s end (Natsume Soseki), A friend has come and is now leaving, Eating persimmons (Masaoka Shiki), 64 CHARLES O\u27KEEFE: Photo, 65 JOHN BURZYNSKI, MEGAN FETTER (Translator): Home is where the heart is, 66 RICHARD BANAHAN: Photo, 67 KIM FREEMAN: Baltimore, 68 JACOB RIDRIGUEZ-NOBLE: Home (Heimat), 69 SUZANNE KENNEDY: Oft verberge ich mich (Oft I hide myself), 70 RICHARD BANAHAN: Photo, 7

    The James Webb Space Telescope Mission

    Full text link
    Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least 4m4m. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the 6.5m6.5m James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

    Supplement: "Localization and broadband follow-up of the gravitational-wave transient GW150914" (2016, ApJL, 826, L13)

    Get PDF
    This Supplement provides supporting material for Abbott et al. (2016a). We briefly summarize past electromagnetic (EM) follow-up efforts as well as the organization and policy of the current EM follow-up program. We compare the four probability sky maps produced for the gravitational-wave transient GW150914, and provide additional details of the EM follow-up observations that were performed in the different bands

    Whole-genome sequencing reveals host factors underlying critical COVID-19

    Get PDF
    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Genetic mechanisms of critical illness in COVID-19.

    Get PDF
    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

    Localization and broadband follow-up of the gravitational-wave transient GW150914

    Get PDF
    A gravitational-wave (GW) transient was identified in data recorded by the Advanced Laser Interferometer Gravitational-wave Observatory (LIGO) detectors on 2015 September 14. The event, initially designated G184098 and later given the name GW150914, is described in detail elsewhere. By prior arrangement, preliminary estimates of the time, significance, and sky location of the event were shared with 63 teams of observers covering radio, optical, near-infrared, X-ray, and gamma-ray wavelengths with ground- and space-based facilities. In this Letter we describe the low-latency analysis of the GW data and present the sky localization of the first observed compact binary merger. We summarize the follow-up observations reported by 25 teams via private Gamma-ray Coordinates Network circulars, giving an overview of the participating facilities, the GW sky localization coverage, the timeline, and depth of the observations. As this event turned out to be a binary black hole merger, there is little expectation of a detectable electromagnetic (EM) signature. Nevertheless, this first broadband campaign to search for a counterpart of an Advanced LIGO source represents a milestone and highlights the broad capabilities of the transient astronomy community and the observing strategies that have been developed to pursue neutron star binary merger events. Detailed investigations of the EM data and results of the EM follow-up campaign are being disseminated in papers by the individual teams

    Whole-genome sequencing reveals host factors underlying critical COVID-19

    Get PDF
    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
    corecore