Basic life support training programme in schools by school nurses: how long and how often to train?

Background: Cardiopulmonary resuscitation (CPR) training in schools, despite being legislated in Spain, is not established as such within the subjects that children are taught in schools. Objective: to evaluate the acquisition of CPR skills by 11-year-old children after a brief theoretical-practical teaching programme taught by nurses at school. Methods: 62 students were assessed in a quasi-experimental study on 2 cohorts (51.4% of the sample in control group [CG]). In total, 2 sessions were given, a theoretical one, and a practical training for skill development in children, in which the CG performed the CPR in 2-minute cycles and the intervention group in 1-minute cycles. The anthropometric variables recorded were weight and height, and the variables compression quality and ventilation quality were recorded using the Laerdal ResusciAnne manikin with Personal Computer/Wireless SkillReport. Results: The assessment showed better results, in terms of BLS sequence performance and use of automated external defibrillator, in the CG and after training, except for the evaluation of the 10-second breathing assessment technique. The quality of chest compressions was better in the CG after training, as was the quality of the ventilations. There were no major differences in CPR quality after training and 4 months after the 1-minute and 2-minute training cycles. Conclusions: 11-year-old children do not perform quality chest compressions or ventilations but, considering their age, they are able to perform a BLS sequence correctly

Prognostic Value of the PROFUND Index for 30-Day Mortality in Acute Heart Failure

Background and Objectives: The prevalence and incidence of heart failure (HF) have been increasing in recent years as the population ages. These patients show a distinct profile of comorbidity, which makes their care more complex. In recent years, the PROFUND index, a specific tool for estimating the mortality rate at one year in pluripathology patients, has been developed. The aim of this study was to evaluate the prognostic value of the PROFUND index and of in-hospital and 30-day mortality after discharge of patients admitted for acute heart failure (AHF). Materials and Methods: A prospective multicenter longitudinal study was performed that included patients admitted with AHF and ≥2 comorbid conditions. Clinical, analytical, and prognostic variables were collected. The PROFUND index was collected in all patients and rates of in-hospital and 30-day mortality after discharge were analyzed. A bivariate analysis was performed with quantitative variables between patients who died and those who survived at the 30-day follow-up. A logistic regression analysis was performed with the variables that obtained statistical significance in the bivariate analysis between deceased and surviving subjects. Results: A total of 128 patients were included. Mean age was 80.5 +/− 9.98 years, and women represented 51.6%. The mean PROFUND index was 5.26 +/− 4.5. The mortality rate was 8.6% in-hospital and 20.3% at 30 days. Preserved left ventricular ejection fraction was found in 60.9%. In the sample studied, there were patients with a PROFUND score < 7 predominated (89 patients (70%) versus 39 patients (31%) with a PROFUND score ≥ 7). Thirteen patients (15%) with a PROFUND score < 7 died versus the 13 (33%) with a PROFUND score ≥ 7, p = 0.03. Twelve patients (15%) with a PROFUND score < 7 required readmission versus 12 patients (35%) with a PROFUND score ≥ 7, p = 0.02. The ROC curve of the PROFUND index for in-hospital mortality and 30-day follow-up in patients with AHF showed AUC 0.63, CI: 95% (0.508–0.764), p <0.033. Conclusions: The PROFUND index is a clinical tool that may be useful for predicting short-term mortality in elderly patients with AHF. Further studies with larger simple sizes are required to validate these results

Clonal chromosomal mosaicism and loss of chromosome Y in elderly men increase vulnerability for SARS-CoV-2

The pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, COVID-19) had an estimated overall case fatality ratio of 1.38% (pre-vaccination), being 53% higher in males and increasing exponentially with age. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, we found 133 cases (1.42%) with detectable clonal mosaicism for chromosome alterations (mCA) and 226 males (5.08%) with acquired loss of chromosome Y (LOY). Individuals with clonal mosaic events (mCA and/or LOY) showed a 54% increase in the risk of COVID-19 lethality. LOY is associated with transcriptomic biomarkers of immune dysfunction, pro-coagulation activity and cardiovascular risk. Interferon-induced genes involved in the initial immune response to SARS-CoV-2 are also down-regulated in LOY. Thus, mCA and LOY underlie at least part of the sex-biased severity and mortality of COVID-19 in aging patients. Given its potential therapeutic and prognostic relevance, evaluation of clonal mosaicism should be implemented as biomarker of COVID-19 severity in elderly people. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, individuals with clonal mosaic events (clonal mosaicism for chromosome alterations and/or loss of chromosome Y) showed an increased risk of COVID-19 lethality

[Correspondencia de Camilo Díaz Baliño] , [19?- 19?]

Mss. autógrafiado e mecanografiadoResumen: Correspondencia sen datas recibida por Camilo Díaz Baliño relacionadas con asuntos persoais e laboraisBiblioteca de GaliciaForma de ingreso: Depósito. Fuente de ingreso: Díaz Pardo, Isaac. Fecha de ingreso: 2011. Propietario: Herdeiros de Isaac Díaz PardoDixitalización Telefónica-IDP 2012Contén : Cartas de: Ramón Domínguez (2 páxs.) -- Bouza Brey (2 páxs.),(2 páxs.) -- Ramón Cabanillas (2 páxs.) -- Castelao (2 páxs.),(2 páxs.),(2 páx.),(1 páx.),(2 páxs.) --María Costa de Porto (2 páxs.)-- Ricardo,Diputación Provincial de La Coruña (2 páxs.)-- Fernández Silva,(2 páx.),(1 fotocopia)-- Antonio Ferrín (1 páx.) -- Juventud Antoniana (1 páx.)-- Agustín Nuñez Díaz (1 páx.)-- J. Portal Fradejas (1 páx.)-- Manuel Ramallo (2 páxs.)-- Antonio Rey Soto (3 páxs.)-- Centro Republicano Radical de Santiago (1 páx.)-- Anónimo (1 páx

GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

Data availability: Downloadable summary data are available through the GenOMICC data site (https://genomicc.org/data). Summary statistics are available, but without the 23andMe summary statistics, except for the 10,000 most significant hits, for which full summary statistics are available. The full GWAS summary statistics for the 23andMe discovery dataset will be made available through 23andMe to qualified researchers under an agreement with 23andMe that protects the privacy of the 23andMe participants. For further information and to apply for access to the data, see the 23andMe website (https://research.23andMe.com/dataset-access/). All individual-level genotype and whole-genome sequencing data (for both academic and commercial uses) can be accessed through the UKRI/HDR UK Outbreak Data Analysis Platform (https://odap.ac.uk). A restricted dataset for a subset of GenOMICC participants is also available through the Genomics England data service. Monocyte RNA-seq data are available under the title ‘Monocyte gene expression data’ within the Oxford University Research Archives (https://doi.org/10.5287/ora-ko7q2nq66). Sequencing data will be made freely available to organizations and researchers to conduct research in accordance with the UK Policy Framework for Health and Social Care Research through a data access agreement. Sequencing data have been deposited at the European Genome–Phenome Archive (EGA), which is hosted by the EBI and the CRG, under accession number EGAS00001007111.Extended data figures and tables are available online at https://www.nature.com/articles/s41586-023-06034-3#Sec21 .Supplementary information is available online at https://www.nature.com/articles/s41586-023-06034-3#Sec22 .Code availability: Code to calculate the imputation of P values on the basis of SNPs in linkage disequilibrium is available at GitHub (https://github.com/baillielab/GenOMICC_GWAS).Acknowledgements: We thank the members of the Banco Nacional de ADN and the GRA@CE cohort group; and the research participants and employees of 23andMe for making this work possible. A full list of contributors who have provided data that were collated in the HGI project, including previous iterations, is available online (https://www.covid19hg.org/acknowledgements).Change history: 11 July 2023: A Correction to this paper has been published at: https://doi.org/10.1038/s41586-023-06383-z. -- In the version of this article initially published, the name of Ana Margarita Baldión-Elorza, of the SCOURGE Consortium, appeared incorrectly (as Ana María Baldion) and has now been amended in the HTML and PDF versions of the article.Copyright © The Author(s) 2023, Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown1 to be highly efficient for discovery of genetic associations2. Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group3. Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling (JAK1), monocyte–macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A).GenOMICC was funded by Sepsis Research (the Fiona Elizabeth Agnew Trust), the Intensive Care Society, a Wellcome Trust Senior Research Fellowship (to J.K.B., 223164/Z/21/Z), the Department of Health and Social Care (DHSC), Illumina, LifeArc, the Medical Research Council, UKRI, a BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070 and BBS/E/D/30002275) and UKRI grants MC_PC_20004, MC_PC_19025, MC_PC_1905 and MRNO2995X/1. A.D.B. acknowledges funding from the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z), the Edinburgh Clinical Academic Track (ECAT) programme. This research is supported in part by the Data and Connectivity National Core Study, led by Health Data Research UK in partnership with the Office for National Statistics and funded by UK Research and Innovation (grant MC_PC_20029). Laboratory work was funded by a Wellcome Intermediate Clinical Fellowship to B.F. (201488/Z/16/Z). We acknowledge the staff at NHS Digital, Public Health England and the Intensive Care National Audit and Research Centre who provided clinical data on the participants; and the National Institute for Healthcare Research Clinical Research Network (NIHR CRN) and the Chief Scientist’s Office (Scotland), who facilitate recruitment into research studies in NHS hospitals, and to the global ISARIC and InFACT consortia. GenOMICC genotype controls were obtained using UK Biobank Resource under project 788 funded by Roslin Institute Strategic Programme Grants from the BBSRC (BBS/E/D/10002070 and BBS/E/D/30002275) and Health Data Research UK (HDR-9004 and HDR-9003). UK Biobank data were used in the GSMR analyses presented here under project 66982. The UK Biobank was established by the Wellcome Trust medical charity, Medical Research Council, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has also had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. The work of L.K. was supported by an RCUK Innovation Fellowship from the National Productivity Investment Fund (MR/R026408/1). J.Y. is supported by the Westlake Education Foundation. SCOURGE is funded by the Instituto de Salud Carlos III (COV20_00622 to A.C., PI20/00876 to C.F.), European Union (ERDF) ‘A way of making Europe’, Fundación Amancio Ortega, Banco de Santander (to A.C.), Cabildo Insular de Tenerife (CGIEU0000219140 ‘Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19’ to C.F.) and Fundación Canaria Instituto de Investigación Sanitaria de Canarias (PIFIISC20/57 to C.F.). We also acknowledge the contribution of the Centro National de Genotipado (CEGEN) and Centro de Supercomputación de Galicia (CESGA) for funding this project by providing supercomputing infrastructures. A.D.L. is a recipient of fellowships from the National Council for Scientific and Technological Development (CNPq)-Brazil (309173/2019-1 and 201527/2020-0)