A Sage for the Age : portrait :Bernard Lewis

Donated by Klaus Kreise

The Correspondence of Shelby Foote & Walker Percy

Letters by Shelby Foote and Walker Percy; edited by Jay Tolson W.W. Norton (Hardcover, $29.95, ISBN: 0393040313, 11/1996; Paperback,$14.00, ISBN: 0393317684, 5/1998) Tolson marshals a more comprehensive selection of the 1948-90 correspondence excerpted in his Percy biography, Pilgrim in the Ruins (1992). Percy\u27s reputation rests on his novels, especially the National Book Award-winning The Moviegoer and Love in the Ruins, Foote\u27s on his titanic nonfiction narrative The Civil War. Because literary orthodoxy beholds Percy as the brighter star, it\u27s surprising how much more brilliantly Foote shines here. Though younger by six months, Foote, who published four novels by age 35, is initially a kind of artistic big brother to Percy, who in 1948 began the first of two novels that preceded The Moviegoer. Since Foote didn\u27t save Percy\u27s letters until 1970, the first 22 years are one-sided: Foote\u27s expansive, 19th-century epistolary style (he recaps Percy\u27s philosophical and artistic arguments as he refutes them) is nearly detailed enough to carry the monologue, and his passion―for writing, reading, music, food―is more than up to the task. However, better annotation from Tolson (as well as a fuller introduction that would put their works in a sequential context) would have shed some welcome light. Even as Percy\u27s star rises, his letters―shorter, less composed, and less frequent―reveal a more tentative, self-doubting muse compared with the brimming confidence that propels Foote fearlessly into his 1.5-million-word magnum opus. Beneath the deeply abiding fraternal affection of boyhood friends (they met at 14 in Greenville, Miss.) lie diametrical approaches to art. Foote, driven to tell stories because how a thing happens is more interesting than what happens or why, advises the christian existentialist (as Percy ruefully considered himself pigeonholed) to leave psychology to the psychologists, theology to the theologians. Percy saves his didacticism for fiction, while Foote continuously assails his friend with literary advice and books to read―most prominently Proust, whom Percy resists to the end. Despite shortcomings in the editorial packaging, the letters provide a fascinating window into a lifelong friendship and the writing life. (8 pages photos) ―Copyright © 1996, Kirkus Associates, LP. All rights reserved.https://egrove.olemiss.edu/mwp_books/1342/thumbnail.jp

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