{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Laursen TL"],"funding":["Danish Council for Independent Research - Medical Sciences","NOVO Nordisk Foundation","NIDDK NIH HHS","National Institutes of Health","Novo Nordisk Fonden"],"pagination":["756-63"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4329085"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["35(3)"],"pubmed_abstract":["<h4>Background & aims</h4>The complement system is activated in liver diseases including acute liver failure (ALF); however, the role of the lectin pathway of complement has scarcely been investigated in ALF. The pathway is initiated by soluble pattern recognition molecules: mannan-binding lectin (MBL), M-, L-, and H-ficolin and collectin-liver-1 (CL-L1), which are predominantly synthesized in the liver. We aimed to study lectin levels in ALF patients and associations with clinical outcome.<h4>Methods</h4>Serum samples from 75 patients enrolled by the US ALF Study Group were collected on days 1 and 3. We included 75 healthy blood donors and 20 cirrhosis patients as controls. Analyses were performed using sandwich-type immunoassays (ELISA, TRIFMA).<h4>Results</h4>At day 1, the MBL level in "],"journal":["Liver international : official journal of the International Association for the Study of the Liver"],"pubmed_title":["Circulating mannan-binding lectin, M-, L-, H-ficolin and collectin-liver-1 levels in patients with acute liver failure."],"pmcid":["PMC4329085"],"funding_grant_id":["U01-DK-58369","12-132318","NNF10OC1013267","U01 DK058369","NNF13OC0007989"],"pubmed_authors":["Prosser C","Lalani E","Larson AM","Vilstrup H","Laursen TL","Taylor W","Senkbeil L","Bernard T","Hay J","McGuire B","Thiel S","Pezzia C","Reuben A","Emre S","Ingram K","Gronbaek H","Murray N","Fontana RJ","Stoy S","Polson J","Munoz S","Welch S","Sandahl TD","Zaman A","Reddy R","Coultrup S","Satyanarayana R","Rush R","Davern TJ","Misra C","McCashland TM","Gottstein J","Avant L","Peacock V","Groettum C","Shakil A","US Acute Liver Failure Study Group","Crippin JS","Hassenein T","Han S","Schiodt FV","Gerstle L","Casson D","Schilsky M","Huntley N","Reisch JS","Harrison M","Partovi K","Barakat F","Blei AT","Lee WM","Chung R","Salvatori J","Smith A","Schwartz J","Rossaro L","Morton D","Campbell M","Stravitz T","Hynan LS","Brown R"],"additional_accession":[]},"is_claimable":false,"name":"Circulating mannan-binding lectin, M-, L-, H-ficolin and collectin-liver-1 levels in patients with acute liver failure.","description":"<h4>Background & aims</h4>The complement system is activated in liver diseases including acute liver failure (ALF); however, the role of the lectin pathway of complement has scarcely been investigated in ALF. The pathway is initiated by soluble pattern recognition molecules: mannan-binding lectin (MBL), M-, L-, and H-ficolin and collectin-liver-1 (CL-L1), which are predominantly synthesized in the liver. We aimed to study lectin levels in ALF patients and associations with clinical outcome.<h4>Methods</h4>Serum samples from 75 patients enrolled by the US ALF Study Group were collected on days 1 and 3. We included 75 healthy blood donors and 20 cirrhosis patients as controls. Analyses were performed using sandwich-type immunoassays (ELISA, TRIFMA).<h4>Results</h4>At day 1, the MBL level in ","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Mar","modification":"2025-04-04T14:39:41.752Z","creation":"2019-03-27T01:45:15Z"},"accession":"S-EPMC4329085","cross_references":{"pubmed":["25203057"],"doi":["10.1111/liv.12682"]}}