The Vehicle, Fall 1992

Table of Contents DeconstructivismPeter F. Essigpage 5 Homecoming Pep RallyPeter F. Essigpage 6 McAfee GymnasiumWalt Howardpage 7 Morton ParkAnn Moutraypage 9 Why The Willows WeepPeter F. Essigpage 10 UntitledStephen P. Carmodypage 10 A Stranger\u27s MorningBen Hausmannpage 11 deMONSTERative pronounsJoAnna Wolaverpage 12 2.5%Jill S. Pilonpage 13 The BottleStacey Kruegerpage 14 Suppression Jean K. Graypage 15 ProgressStacey Kruegerpage 16 Daily LessonsJennifer Moropage 17 Sunset TheaterMichelle R. Hokepage 20 Eagle GT\u27sJarrod T. Shieldspage 21 New HouseRandy Lisspage 22 UntitledStephen P. Carmodypage 23 Renting Classics on a Saturday NightNancy Jamespage 24 UntitledJacqueline Hallpage 25 Alone While He SleepsSandy Beauchamppage 26 Sand and SeaThomas Schnarrepage 27 loveMichelle R. Hokepage 28 Backward Ass Junkie FunkSandy Beauchamppage 28 These Things You KeepTom McGrathpage 29 Springhill CrestRobert M. Reutherpage 30 The Pass OverLarry Irvinpage 31 The Stolen ChildTom McGrathpage 32 Before the Recycling KickWalt Howardpage 37 Authors\u27 Pagepage 38https://thekeep.eiu.edu/vehicle/1058/thumbnail.jp

Nucleo-cytoplasmic transport of proteins and RNA in plants

Merkle T. Nucleo-cytoplasmic transport of proteins and RNA in plants. Plant Cell Reports. 2011;30(2):153-176.Transport of macromolecules between the nucleus and the cytoplasm is an essential necessity in eukaryotic cells, since the nuclear envelope separates transcription from translation. In the past few years, an increasing number of components of the plant nuclear transport machinery have been characterised. This progress, although far from being completed, confirmed that the general characteristics of nuclear transport are conserved between plants and other organisms. However, plant-specific components were also identified. Interestingly, several mutants in genes encoding components of the plant nuclear transport machinery were investigated, revealing differential sensitivity of plant-specific pathways to impaired nuclear transport. These findings attracted attention towards plant-specific cargoes that are transported over the nuclear envelope, unravelling connections between nuclear transport and components of signalling and developmental pathways. The current state of research in plants is summarised in comparison to yeast and vertebrate systems, and special emphasis is given to plant nuclear transport mutants

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 hospitalization2–4 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

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

Development and pilot testing of a decision aid for drivers with dementia

Background An increasing number of older adults drive automobiles. Given that the prevalence of dementia is rising, it is necessary to address the issue of driving retirement. The purpose of this study is to evaluate how a self-administered decision aid contributed to decision making about driving retirement by individuals living with dementia. The primary outcome measure in this study was decisional conflict. Knowledge, decision, satisfaction with decision, booklet use and booklet acceptability were the secondary outcome measures. Methods A mixed methods approach was adopted. Drivers with dementia were recruited from an Aged Care clinic and a Primary Care center in NSW, Australia. Telephone surveys were conducted before and after participants read the decision aid. Results Twelve participants were recruited (mean age 75, SD 6.7). The primary outcome measure, decisional conflict, improved following use of the decision aid. Most participants felt that the decision aid: (i) was balanced; (ii) presented information well; and (iii) helped them decide about driving. In addition, mean knowledge scores improved after booklet use. Conclusions This decision aid shows promise as an acceptable, useful and low-cost tool for drivers with dementia. A self-administered decision aid can be used to assist individuals with dementia decide about driving retirement. A randomized controlled trial is underway to evaluate the effectiveness of the tool