15 research outputs found

    Justice for children in healthcare: an asymmetric theory of responsibility/Justicia para los niños en el sistema sanitario: una teoría asimétrica de la responsabilidad

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    Healthcare providers face enormous pressure to save healthcare resources where possible. In this paper I explore the response that we should allocate resources fairly. What is a fair allocation of healthcare resources for children? First, I consider the luck egalitarianism approach of limiting resources to adult patients who are responsible for their conditions. A luck egalitarian distribution of healthcare resources to adults faces significant problems in application. I maintain that when we consider these problems with a focus on the just distribution of health-care resources to children, we gain valuable insights into the fairness of healthcare allocation for adults

    Justice for children in healthcare: an asymmetric theory of responsibility/Justicia para los niños en el sistema sanitario: una teoría asimétrica de la responsabilidad

    Get PDF
    Healthcare providers face enormous pressure to save healthcare resources where possible. In this paper I explore the response that we should allocate resources fairly. What is a fair allocation of healthcare resources for children? First, I consider the luck egalitarianism approach of limiting resources to adult patients who are responsible for their conditions. A luck egalitarian distribution of healthcare resources to adults faces significant problems in application. I maintain that when we consider these problems with a focus on the just distribution of health-care resources to children, we gain valuable insights into the fairness of healthcare allocation for adults

    Fairness as “appropriate impartiality” and the problem of the self-serving bias

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    Garrett Cullity contends that fairness is appropriate impartiality (See Cullity (2004) Chapters 8 and 10 and Cullity (2008)). Cullity deploys his account of fairness as a means of limiting the extreme moral demand to make sacrifices in order to aid others that was posed by Peter Singer in his seminal article ‘Famine, Affluence and Morality’. My paper is founded upon the combination of (1) the observation that the idea that fairness consists in appropriate impartiality is very vague and (2) the fact that psychological studies show the self-serving bias is especially likely to infect one’s judgements when the ideas involved are vague. I argue that Cullity’s solution to extreme moral demandingness is threatened by these findings. I then comment on whether some other theories of fairness are vulnerable to the same objection

    Genetic mechanisms of critical illness in COVID-19.

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    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

    Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity

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    The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)
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