1923 - A.C.C Bible Lecture Week, Abilene Christian College

This is program for the 1923 Sixth Annual Bible Lecture Week at Abilene Christian College. Uploaded by Jackson Hager

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

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

Use of enzymatic methods for rapid enumeration of coliforms in freshwaters

Rapid enumeration methods based on the enzymatic hydrolysis of 4-methylumbelliferyl-β- d-galactoside and 4-methylumbelliferyl-β- d-glucuronide were optimized for freshwaters. The enzymes β- d-galactosidase (GALase) and β- d-glucuronidase (GLUase) were shown to be already induced in freshwaters when tested, respectively, with the inducers isopropyl-β- d-thiogalactopyranoside and methyl-β- d-glucuronide. Both enzymatic activities were compared, respectively, with plate counts of total and faecal coliforms in freshwaters. Enzymatic methods and reference plate counts were significantly correlated in log–log plots. Moreover, the GLUase method allowed the detection of viable (presenting a detectable GLUase activity) but nonculturable Escherichia coli.FLWINinfo:eu-repo/semantics/publishe