14 research outputs found

    Residual lung abnormalities following COVID-19 hospitalisation: interim analysis of the UKILD Post-COVID study

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    Rationale: shared symptoms and genetic architecture between COVID-19 and lung fibrosis suggests SARS-CoV-2 infection may lead to progressive lung damage.Objectives: the UKILD Post-COVID study interim analysis was planned to estimate the prevalence of residual lung abnormalities in people hospitalised with COVID-19 based on risk strata.Methods: the Post-HOSPitalisation COVID Study (PHOSP-COVID) was used for capture of routine and research follow-up within 240 days from discharge. Thoracic CTs were linked by PHOSP-COVID identifiers and scored for percentage involvement of residual abnormalities (ground glass opacities and reticulations). Risk factors in linked CT were estimated with Bayesian binomial regression and used to generate risk strata. Numbers of cases within strata were used to estimate post-hospitalisation prevalence using Bayesian binomial distributions. Sensitivity was performed in research follow-up participants.Measurements and Main Results: the interim cohort comprised 3700 people. Of 209 linked CTs (median 119 days, interquartile range 83-155), 164 people (79.6%) had &gt;10% involvement of residual lung abnormalities. Major risk factors included abnormal chest X-ray (RR 1·21 95%CrI 1·05; 1·40), percent predicted DLco&lt;80% (RR 1·25 95%CrI 1·00; 1·56) and severe admission requiring ventilation support (RR 1·27 95%CrI 1·07; 1·55). Moderate to very-high risk was classified in 7·8% of the remaining 3491 people, post-hospitalisation prevalence was estimated at 8.5% (95%CI CrI 7.6%; 9.5%) rising to 11.7% (95%CrI 10.3%; 13.1%) in sensitivity analysis.Conclusions: prevalence of residual lung abnormalities were estimated in up to 11% of people discharged following COVID-19 related hospitalisation. Health services should monitor at-risk individuals to elucidate long term functional implications.<br/

    Complement factor H: using atomic resolution structure to illuminate disease mechanisms.

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    Complement Factor H has recently come to the fore with variant forms implicated in a range of serious disease states. This review aims to bring together recent data concerning the structure and biological activity of this molecule to highlight the way in which a molecular understanding of function may open novel therapeutic possibilities. In particular we examine the evidence for and against the hypothesis that sequence variations in factor H may predispose to disease if they perturb its ability to recognise and respond appropriately to polyanionic carbohydrates on host surfaces that require protection from complement-mediated damage

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    Mapping autism risk loci using genetic linkage and chromosomal rearrangements

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    Autism spectrum disorders (ASDs) are common, heritable neurodevelopmental conditions. The genetic architecture of ASDs is complex, requiring large samples to overcome heterogeneity. Here we broaden coverage and sample size relative to other studies of ASDs by using Affymetrix 10K SNP arrays and 1,168 families with at least two affected individuals, performing the largest linkage scan to date while also analyzing copy number variation in these families. Linkage and copy number variation analyses implicate chromosome 11p12-p13 and neurexins, respectively, among other candidate loci. Neurexins team with previously implicated neuroligins for glutamatergic synaptogenesis, highlighting glutamate-related genes as promising candidates for contributing to ASDs. © 2007 Nature Publishing Group

    Phylum XIV. Bacteroidetes phyl. nov.

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