<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Stanojcic M</submitter><funding>NIGMS NIH HHS</funding><funding>CIHR</funding><pagination>1357-64</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4166573</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(6)</volume><pubmed_abstract>&lt;h4>Objectives&lt;/h4>Severe thermal injury is associated with extreme and prolonged inflammatory and hypermetabolic responses, resulting in significant catabolism that delays recovery or even leads to multiple organ failure and death. Burned patients exhibit many symptoms of stress-induced diabetes, including hyperglycemia, hyperinsulinemia, and hyperlipidemia. Recently, the nucleotide-binding domain, leucine-rich family (NLR), pyrin-containing 3 (NLRP3) inflammasome has received much attention as the sensor of endogenous "danger signals" and mediator of "sterile inflammation" in type II diabetes. Therefore, we investigated whether the NLRP3 inflammasome is activated in the adipose tissue of burned patients, as we hypothesize that, similar to the scenario observed in chronic diabetes, the cy</pubmed_abstract><journal>Critical care medicine</journal><pubmed_title>Leukocyte infiltration and activation of the NLRP3 inflammasome in white adipose tissue following thermal injury.</pubmed_title><pmcid>PMC4166573</pmcid><funding_grant_id>123336</funding_grant_id><funding_grant_id>R01 GM087285-01</funding_grant_id><funding_grant_id>R01 GM087285</funding_grant_id><pubmed_authors>Zuniga-Pflucker JC</pubmed_authors><pubmed_authors>Harrison RA</pubmed_authors><pubmed_authors>Antonyshyn J</pubmed_authors><pubmed_authors>Chen P</pubmed_authors><pubmed_authors>Stanojcic M</pubmed_authors><pubmed_authors>Jeschke MG</pubmed_authors><pubmed_authors>Wang V</pubmed_authors></additional><is_claimable>false</is_claimable><name>Leukocyte infiltration and activation of the NLRP3 inflammasome in white adipose tissue following thermal injury.</name><description>&lt;h4>Objectives&lt;/h4>Severe thermal injury is associated with extreme and prolonged inflammatory and hypermetabolic responses, resulting in significant catabolism that delays recovery or even leads to multiple organ failure and death. Burned patients exhibit many symptoms of stress-induced diabetes, including hyperglycemia, hyperinsulinemia, and hyperlipidemia. Recently, the nucleotide-binding domain, leucine-rich family (NLR), pyrin-containing 3 (NLRP3) inflammasome has received much attention as the sensor of endogenous "danger signals" and mediator of "sterile inflammation" in type II diabetes. Therefore, we investigated whether the NLRP3 inflammasome is activated in the adipose tissue of burned patients, as we hypothesize that, similar to the scenario observed in chronic diabetes, the cy</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jun</publication><modification>2025-06-26T03:05:23.31Z</modification><creation>2025-06-26T03:05:23.31Z</creation></dates><accession>S-EPMC4166573</accession><cross_references><pubmed>24584061</pubmed><doi>10.1097/ccm.0000000000000209</doi><doi>10.1097/CCM.0000000000000209</doi></cross_references></HashMap>