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Genetic mechanisms of critical illness in Covid-19

四川生理科学杂志 2020年第4期42卷 455-455页

作者： Erola Pairo-Castineira Roslin Institute University of Edinburgh Edinburgh UK MRC Human Genetics Unit Institute of Genetics and Molecular Medicine University of Edinburgh Western General Hospital Edinburgh UK Genomics England London UK Centre for Inflammation Research The Queen’s Medical Research Institute University of Edinburgh Edinburgh UK Centre for Genomic and Experimental Medicine Institute of Genetics and Molecular Medicine University of Edinburgh Western General Hospital Edinburgh UK Edinburgh Clinical Research Facility Western General Hospital University of Edinburgh Edinburgh UK Intensive Care National Audit & Research Centre London UK Institute for Molecular Bioscience The University of Queensland Brisbane Australia Biostatistics Group School of Life Sciences Sun Yat-sen University Guangzhou China The Crick Institute London UK Intensive Care Unit Royal Infirmary of Edinburgh Edinburgh UK School of Life Sciences Westlake University Hangzhou China Westlake laboratory of Life Sciences and Biomedicine Hangzhou China Wellcome Centre for Human Genetics University of Oxford Oxford UK Department of Medicine University of Cambridge Cambridge UK Department of Intensive Care Medicine Guy’s and St Thomas’ NHS Foundation Trust London UK School of Immunology and microbial Sciences King’s College London London UK NIHR Health Protection Research Unit for Emerging and Zoonotic Infections Institute of Infection Veterinary and Ecological Sciences University of Liverpool Liverpool UK MRC-University of Glasgow Centre for Virus Research Institute of Infection Immunity and Inflammation College of Medical Veterinary and Life Sciences University of Glasgow Glasgow UK William Harvey Research Institute Barts and the London School of Medicine and Dentistry Queen Mary University of London London UK Centre for Tropical Medicine and Global Health Nuffield Department of Medicine University of Oxford Oxford UK Clinical Research Centre at St Vincent’s University Hospital University Col

Host-mediated lung inflammation is present,1 and drives mortality,2 in critical illness caused by *** genetic variants associated with critical illness may identify mechanistic targets for therapeutic development.3 Here we report the results of the GenOMICC(Genetics Of Mortality In Critical Care)genome-wide association study(GWAS)in 2244 critically ill Covid-19 patients from 208 UK intensive care units(ICUs).We identify and replicate novel genome-wide significant associations,on chr12q24.13(rs10735079,p=1.65[Formula:see text]10-8)in a gene cluster encoding antiviral restriction enzyme activators(OAS1,OAS2,OAS3),on chr19p13.2(rs2109069,p=2.3[Formula:see text]10-12)near the gene encoding tyrosine kinase 2(TYK2),on chr19p13.3(rs2109069,p=3.98[Formula:see text]10-12)within the gene encoding dipeptidyl peptidase 9(DPP9),and on chr21q22.1(rs2236757,p=4.99[Formula:see text]10-8)in the interferon receptor gene *** identify potential targets for repurposing of licensed medications:using Mendelian randomisation we found evidence in support of a causal link from low expression of IFNAR2,and high expression of TYK2,to life-threatening disease;transcriptome-wide association in lung tissue revealed that high expression of the monocyte/macrophage chemotactic receptor CCR2 is associated with severe *** results identify robust genetic signals relating to key host antiviral defence mechanisms,and mediators of inflammatory organ damage in *** mechanisms may be amenable to targeted treatment with existing ***-scale randomised clinical trials will be essential before any change to clinical practice.

关键词： lung drugs critical

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Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis

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World Journal of Hepatology 2021年第12期13卷 2052-2070页

作者： Larisse Longo Pabulo Henrique Rampelotto Eduardo Filippi-Chiela Valessa Emanoele Gabriel de Souza Fernando Salvati Carlos Thadeu Cerski Themis Reverbel da Silveira Cláudia P Oliveira Carolina Uribe-Cruz Mário ReisÁlvares-da-Silva Experimental laboratory of Hepatology and Gastroenterology Hospital de Clínicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil Graduate Program in Gastroenterology and Hepatology Universidade Federal do Rio Grande do SulPorto Alegre 90035-003Rio Grande do SulBrazil Graduate Program in Genetics and Molecular Biology Universidade Federal do Rio Grande do SulPorto Alegre 90035-903Rio Grande do SulBrazil Center of Biotechnology Universidade Federal do Rio Grande do SulPorto Alegre 91501-970Rio Grande do SulBrazil Department of Morphological Sciences Universidade Federal do Rio Grande do SulPorto Alegre 90050-170Rio Grande do SulBrazil Experimental Research Center Hospital de Clínicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil School of Medicine Instituto Meridional de Educação-IMEDPasso Fundo 99070-220Rio Grande do SulBrazil Unit of Surgical Pathology Hospital de Clínicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil Department of Gastroenterology(LIM07) Faculdade de Medicina da Universidade de São PauloSão Paulo 01246903Brazil Division of Gastroenterology Hospital de Clínicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil

BACKGROUND Cardiovascular disease is the main cause of death in metabolic-associated fatty liver disease,and gut microbiota dysbiosis is associated with both of *** To assess the relationship between gut dysbiosis and cardiovascular risk(CVR)in an experimental model of *** Adult male Sprague-Dawley rats were randomized to a control group(n=10)fed a standard diet and an intervention group(n=10)fed a high-fat choline-deficient diet for 16 ***,molecular,hepatic,and cardiac *** microbiota variables were *** The intervention group had a significantly higher atherogenic coefficient,Castelli’s risk index(CRI)-I and CRI-II,interleukin-1β,tissue inhibitor of metalloproteinase-1(all Pmicrobial families that are involved in lipid metabolism were differentially abundant in intervention group and were significantly correlated with markers of liver injury and *** The study found a link between gut dysbiosis and significant cardiomyocyte abnormalities in animals with steatohepatitis.

关键词： Animal model Cardiovascular diseases Gut microbiota Metabolic-associated fatty liver disease Predicted lipid metabolism Risk cardiovascular Steatohepatitis

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Effect of fiber supplementation on the microbiota in critically ill patients

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World Journal of Gastrointestinal Pathophysiology 2011年第6期2卷 138-145页

作者： Stephen JD O'Keefe Junhai Ou James P DeLany Scott Curry Erwin Zoetendal H Rex Gaskins Scott Gunn Division of Gastroenterology Department of MedicineUniversity of PittsburghPittsburghPA 15213United States Division of Endocrinology Department of MedicineUniversity of PittsburghPittsburghPA 15261United States Division of Infectious Disease Department of MedicineUniversity of PittsburghPittsburghPA 15261United States laboratory of Microbiology Wageningen UniversityWageningen 6703HBThe Netherlands Department of Animal Sciences and Pathobiology Division of Nutritional SciencesInstitute for Genomic BiologyUniversity of Illinois at Urbana-ChampaignUrbanaIL 61801United States Division of Critical Care Medicine Department of MedicineUniversity of PittsburghPittsburghPA 15261United States

AIM:To determine tolerance to fiber supplementation of semi-elemental tube feeds in critically ill patients and measure its effect on colonic microbiota and ***:Thirteen intensive care unit patients receiving jejunal feeding with a semi-elemental diet for predominantly necrotizing pancreatitis were *** study was divided into 2 parts:first,short-term (3-9 d)clinical tolerance and colonic fermentation as assessed by fecal short chain fatty acid(SCFA)concentrations and breath hydrogen and methane was measured in response to progressive fiber supplementation increasing from 4 g tid up to normal requirement levels of 8 g tid;second,4 patients with diarrhea were studied for 2-5 wk with maximal supplementation to additionally assess its influence on fecal microbiota quantitated by quantitative polymerase chain reaction (qPCR)of microbial 16S rRNA genes and Human Intestinal Tract Chip(HITChip)microarray *** all patients were receiving antibiotics(10/13)and acid suppressants(11/13)at some stage during the ***:In group 1,tolerance to progressive fiber supplementation was good with breath hydrogen and methane evidence(P=0.008 and Pmicrobial counts of specific butyrate producers,with resolution of diarrhea in 3 of 4 ***:Conventional management of critically ill patie

关键词： Critical illness Acute pancreatitis Microbiota Enteral nutrition Fiber

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