Comic Iconoclasm

A collection of essays and an historic survey of visual work divided into "characters", "narrative" and "style" as related to 20th Century comic art. The texts accompany comics as seen through the eyes of European and American artists ranging from Dubuffet to Bender. 32 bibl. ref

Like Life : Sculpture, Color, and the Body

"Since the dawn of history, humans have created three-dimensional renderings of the body, and for centuries artists strove for realism, often creating works of stunning verisimilitude and using color to enhance religious, cultural, or personal meaning. This volume examines key sculptural works from 14th century Europe to the global present, revealing new insights into the strategies artists deploy to blur the distinction between art and life." -- publisher's website

Carnegie International 1991

Volume one includes an extended foreword and preface, four essays, and statements by 44 artists; volume two has a fifth essay on the exhibition and installation shots. Subjects covered include the history of the exhibition and the Carnegie museum, curatorial rationale, architecture, postmodernism, hypertravel, language and linguistic theory, internationalism and transculturalism, metaculture, post-communism and contemporary Russian culture, contemporary museology, collection and display ideology. Biographical notes. Bibl. 6 p

The Artist's Joke

"This anthology traces humour's role in transforming the practice and experience of art, from the early twentieth-century avant-gardes, through Fluxus and Pop, to the diverse, often uncategorizable works of some of the most influential artists today" -- p. [4] of cover

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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