<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Rautanen A</submitter><funding>Thuringian Ministry of Education</funding><funding>Wellcome Trust grant reference</funding><funding>European Research Council</funding><funding>Wellcome Trust Core Award Grant Number</funding><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><funding>Wellcome Trust</funding><funding>Federal Ministry of Education and Research</funding><pagination>53-60</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4314768</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>3(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Sepsis continues to be a major cause of death, disability, and health-care expenditure worldwide. Despite evidence suggesting that host genetics can influence sepsis outcomes, no specific loci have yet been convincingly replicated. The aim of this study was to identify genetic variants that influence sepsis survival.&lt;h4>Methods&lt;/h4>We did a genome-wide association study in three independent cohorts of white adult patients admitted to intensive care units with sepsis, severe sepsis, or septic shock (as defined by the International Consensus Criteria) due to pneumonia or intra-abdominal infection (cohorts 1-3, n=2534 patients). The primary outcome was 28 day survival. Results for the cohort of patients with sepsis due to pneumonia were combined in a meta-analysis of 1553 p</pubmed_abstract><journal>The Lancet. Respiratory medicine</journal><pubmed_title>Genome-wide association study of survival from sepsis due to pneumonia: an observational cohort study.</pubmed_title><pmcid>PMC4314768</pmcid><funding_grant_id>ACF-2011-13-004</funding_grant_id><funding_grant_id>0312617</funding_grant_id><funding_grant_id>CL-2006-13-003</funding_grant_id><funding_grant_id>294557</funding_grant_id><funding_grant_id>G1100449</funding_grant_id><funding_grant_id>NIHR/CS/009/007</funding_grant_id><funding_grant_id>B309-00014</funding_grant_id><funding_grant_id>G9521010</funding_grant_id><funding_grant_id>NF-SI-0514-10158</funding_grant_id><funding_grant_id>NF-SI-0512-10113</funding_grant_id><funding_grant_id>G0900747</funding_grant_id><funding_grant_id>MR/K006584/1</funding_grant_id><funding_grant_id>G1001712</funding_grant_id><funding_grant_id>090532/Z/09/Z</funding_grant_id><funding_grant_id>090532/Z/09/Z and MRC Hub grant G0900747 91070</funding_grant_id><pubmed_authors>Sirgo G</pubmed_authors><pubmed_authors>Garrard CS</pubmed_authors><pubmed_authors>Schneider EM</pubmed_authors><pubmed_authors>Hill AV</pubmed_authors><pubmed_authors>Russell JA</pubmed_authors><pubmed_authors>Chapman SJ</pubmed_authors><pubmed_authors>Cotogni P</pubmed_authors><pubmed_authors>Reinhart K</pubmed_authors><pubmed_authors>Holloway PA</pubmed_authors><pubmed_authors>Rautanen A</pubmed_authors><pubmed_authors>Chiche JD</pubmed_authors><pubmed_authors>Russwurm S</pubmed_authors><pubmed_authors>Meitinger T</pubmed_authors><pubmed_authors>Rello J</pubmed_authors><pubmed_authors>Gordon AC</pubmed_authors><pubmed_authors>Mills TC</pubmed_authors><pubmed_authors>Weiss YG</pubmed_authors><pubmed_authors>Knight JC</pubmed_authors><pubmed_authors>Nuamah R</pubmed_authors><pubmed_authors>Elliott KS</pubmed_authors><pubmed_authors>Mein C</pubmed_authors><pubmed_authors>Steffens M</pubmed_authors><pubmed_authors>Hinds CJ</pubmed_authors><pubmed_authors>ESICM/ECCRN GenOSept Investigators</pubmed_authors><pubmed_authors>Sarapuu S</pubmed_authors><pubmed_authors>Hutton P</pubmed_authors><pubmed_authors>Bion J</pubmed_authors><pubmed_authors>Parks T</pubmed_authors><pubmed_authors>Caulfield MJ</pubmed_authors><pubmed_authors>Stuber F</pubmed_authors><pubmed_authors>Davenport EE</pubmed_authors><pubmed_authors>Walley KR</pubmed_authors><pubmed_authors>Wienker TF</pubmed_authors><pubmed_authors>Ranieri VM</pubmed_authors><pubmed_authors>Lichtner P</pubmed_authors><pubmed_authors>Bloos F</pubmed_authors><pubmed_authors>Kobilay M</pubmed_authors><pubmed_authors>Sramek V</pubmed_authors><pubmed_authors>Bobek I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genome-wide association study of survival from sepsis due to pneumonia: an observational cohort study.</name><description>&lt;h4>Background&lt;/h4>Sepsis continues to be a major cause of death, disability, and health-care expenditure worldwide. Despite evidence suggesting that host genetics can influence sepsis outcomes, no specific loci have yet been convincingly replicated. The aim of this study was to identify genetic variants that influence sepsis survival.&lt;h4>Methods&lt;/h4>We did a genome-wide association study in three independent cohorts of white adult patients admitted to intensive care units with sepsis, severe sepsis, or septic shock (as defined by the International Consensus Criteria) due to pneumonia or intra-abdominal infection (cohorts 1-3, n=2534 patients). The primary outcome was 28 day survival. Results for the cohort of patients with sepsis due to pneumonia were combined in a meta-analysis of 1553 p</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jan</publication><modification>2026-04-30T23:37:31.893Z</modification><creation>2019-03-27T01:44:30Z</creation></dates><accession>S-EPMC4314768</accession><cross_references><pubmed>25533491</pubmed><doi>10.1016/S2213-2600(14)70290-5</doi></cross_references></HashMap>