Photographing Turkey Run: A Guide to Nature Photography

Photographing Turkey Run: A Guide to Nature Photography was written to be used in conjunction with Daniel P. Shepardson’s A Place Called Turkey Run: A Celebration of Indiana’s Second State Park in Photographs and Words. This guide contains tips and techniques designed to provide a basic understanding of how to photograph nature and improve one’s photography skills

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

Genetic mechanisms of critical illness in COVID-19.

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

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

Students’ conceptions about the greenhouse effect, global warming, and climate change

The purpose of this study was to investigate students\u27 conceptions of the greenhouse effect, global warming, and climate change. The study was descriptive in nature and reflected a cross-age design involving the collection of qualitative data from 51 secondary students from three different schools in the Midwest, USA. These data were analyzed for content in an inductive manner to identify student\u27s conceptions. The categories that emerged from the students\u27 responses reflected different degrees of sophistication of students\u27 conceptions about the greenhouse effect, global warming, and climate change. Based on these findings we make curricular recommendations that build on the students\u27 conceptions, the IPCC Findings, the NRC (1996) science education standards, and NOAA\u27s climate literacy framework

Do Earth anD EnvironmEntal SciEncE tExtbookS PromotE miDDlE anD high School StuDEntS’concEPtual DEvEloPmEnt about climatE changE?

Misconceptions or a lack of relevant prior concepts can hinder students from developing an understanding of scientific concepts. Science education research suggests that building on students\u27 prior concepts is an effective way to develop students\u27 scientific knowledge. This study reports the results of an analysis of earth and environmental science textbooks\u27 representations of climate change concepts and an examination of these presentations for possible contribution to students\u27 common misconceptions of climate change. A literature review was conducted to identify students\u27 common misconceptions of climate change. Textbooks\u27 conceptual coverage and their ways of presenting scientific conceptions were examined concerning their potential influence on further reinforcing and adding greater confidence to students\u27 misconceptions. Our results indicate that the reviewed textbooks were not designed based on careful consideration of students\u27 common misconceptions of climate change. We made recommendations for improving the conceptual clarity and organization of climate change concepts in Earth and environmental science textbooks

Seventh grade students\u27 mental models of the greenhouse effect

This constructivist study investigates 225 student drawings and explanations from three different schools in the midwest in the US, to identify seventh grade students\u27 mental models of the greenhouse effect. Five distinct mental models were derived from an inductive analysis of the content of the students\u27 drawings and explanations: Model 1, a \u27greenhouse\u27 for growing plants; Model 2, greenhouse gases cause ozone depletion or formation, causing the Earth to warm; Model 3, greenhouse gases, but no heating mechanism, simply gases in the atmosphere; Model 4, greenhouse gases \u27trap\u27 the sun\u27s rays, heating the Earth; and Model 5, the sun\u27s rays are \u27bounced\u27 or reflected back and forth between the Earth\u27s surface and greenhouse gases, heating the Earth. Science textbooks are critiqued in light of the students\u27 mental models and curricular and instructional implications are explored. [ABSTRACT FROM AUTHOR

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease