{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE188nnn/GSE188890/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE188890"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Determining the Translational Potential of Human Pericardial Fluid to Improve Clinical Outcomes in Cardiac Surgery","description":"The pericardial space, which contains pericardial fluid (PF), maintains homeostatic conditions that facilitates optimal heart function. PF can carry biomarkers for different cardiac diseases. PF can also play a central role in delivering targeted therapeutics. The loss of PF during surgery perturbs the equilibrium of this environment, contributing to postsurgical complications, including postoperative pericardial adhesion formation (PPAF) and postoperative atrial fibrillation (POAF), both of which involve immune-mediated pathways. We have yet to fully understand the exact pathophysiology of these adverse events. This study aimed to establish the immune profile of human PF, determine whether specific markers can drive inflammatory processes, such as fibrosis, and elucidate the underlying mechanisms that can result in such phenomena.","dates":{"publication":"2026/07/09"},"accession":"GSE188890","cross_references":{"GSM":["GSM5691539","GSM5691538","GSM5691540","GSM5691542","GSM5691541","GSM5910792","GSM5691537","GSM5691536","GSM6049897"],"GPL":["18573"],"SRA":["SRP346236"],"GSE":["188890"],"taxon":["Homo sapiens"]}}