Evolving modes of student use - whither the VLE?

We consider the issue of where physically Informatics students choose to work. Technological change now offers them a range of points of access, at the same time as institutions are exploiting these modes to the full. In the context of a new institutional VLE, we have conducted a preliminary study of modes of use: we learn, unsurprisingly, that use of central bulk laboratories is diminishing, but that there may be subtle patterns of behaviour evident among individuals. We note that these behaviours are driven by strong external forces and will not be countered, and further note that there may be cause to worry about students becoming ‘virtual’, both for their own academic benefit and their enculturation. We conjecture that conclusions for Informatics will be relevant to the whole academy as time passes, and propose work to monitor this issue

The compensatory potential of increased immigration following intensive American mink population control is diluted by male-biased dispersal

Attempts to mitigate the impact of invasive species on native ecosystems increasingly target large land masses where control, rather than eradication, is the management objective. Depressing numbers of invasive species to a level where their impact on native biodiversity is tolerable requires overcoming the impact of compensatory immigration from non-controlled portions of the landscape. Because of the expected scale-dependency of dispersal, the overall size of invasive species management areas relative to the dispersal ability of the controlled species will determine the size of any effectively conserved core area unaffected by immigration from surrounding areas. However, when dispersal is male-biased, as in many mammalian invasive carnivores, males may be overrepresented amongst immigrants, reducing the potential growth rate of invasive species populations in re-invaded areas. Using data collected from a project that gradually imposed spatially comprehensive control on invasive American mink (Neovison vison) over a 10,000 km2 area of NE Scotland, we show that mink captures were reduced to almost zero in 3 years, whilst there was a threefold increase in the proportion of male immigrants. Dispersal was often long distance and linking adjacent river catchments, asymptoting at 38 and 31 km for males and females respectively. Breeding and dispersal were spatially heterogeneous, with 40 % of river sections accounting for most captures of juvenile (85 %), adult female (65 %) and immigrant (57 %) mink. Concentrating control effort on such areas, so as to turn them into “attractive dispersal sinks” could make a disproportionate contribution to the management of recurrent re-invasion of mainland invasive species management areas

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

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Scattering laws for reflected solar radiation and the characterisation of terrain roughness.

The problems associated with simple models for terrestrial and planetary surface reflectance are discussed and the value of using more rigorous expressions that properly describe the effects of sub-pixel shadowing at low solar zenith angles is emphasised. The use of such expressions will improve the accuracy of theoretical reflectance estimates and could provide information useful in geological mapping, geomorphology, vegetation classification, climatology and micrometeorology. An existing general-purpose roughness correction to radiative transfer models of surface reflectance is considered in some detail, and the relationship of its roughness parameter, θ, to sub-pixel terrain morphology is then explored through the collection and analysis of reflectance measurements from fractal digital terrain models. A well-defined relationship is found to exist between θ and fractal dimension, D, such that, under certain circumstances, knowledge of one may be used to infer the other