<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>15</volume><submitter>Li L</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Disulfidptosis is a recently identified form of cell death that contributes to maintaining the internal environment balance of an organism. However, the molecular basis of disulfidptosis in ulcerative colitis (UC), ankylosing spondylitis (AS), and Crohn's disease (CD) has not been thoroughly explored.&lt;h4>Methods&lt;/h4>Firstly, the differentially expressed genes (DEGs) and disulfidptosis-associated genes (DAGs) were obtained through differential analysis between diseases (AS, CD, and UC) and control groups. After the disulfidptosis score was acquired using the single-sample gene set enrichment analysis (ssGSEA) algorithm, the DE-DAGs were screened by overlapping DAGs and DEGs of the three diseases. Next, the feature genes were selected through a combination of machine lea</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1326354</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10904683</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Regulation mechanisms of disulfidptosis-related genes in ankylosing spondylitis and inflammatory bowel disease.</pubmed_title><pmcid>PMC10904683</pmcid><pubmed_authors>Fang H</pubmed_authors><pubmed_authors>Liping D</pubmed_authors><pubmed_authors>Jin X</pubmed_authors><pubmed_authors>Zhou P</pubmed_authors><pubmed_authors>Xie K</pubmed_authors><pubmed_authors>Song R</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Yang P</pubmed_authors><pubmed_authors>Zhu H</pubmed_authors><pubmed_authors>Li L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation mechanisms of disulfidptosis-related genes in ankylosing spondylitis and inflammatory bowel disease.</name><description>&lt;h4>Introduction&lt;/h4>Disulfidptosis is a recently identified form of cell death that contributes to maintaining the internal environment balance of an organism. However, the molecular basis of disulfidptosis in ulcerative colitis (UC), ankylosing spondylitis (AS), and Crohn's disease (CD) has not been thoroughly explored.&lt;h4>Methods&lt;/h4>Firstly, the differentially expressed genes (DEGs) and disulfidptosis-associated genes (DAGs) were obtained through differential analysis between diseases (AS, CD, and UC) and control groups. After the disulfidptosis score was acquired using the single-sample gene set enrichment analysis (ssGSEA) algorithm, the DE-DAGs were screened by overlapping DAGs and DEGs of the three diseases. Next, the feature genes were selected through a combination of machine lea</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024</publication><modification>2026-07-01T03:22:04.756Z</modification><creation>2025-04-07T04:49:49.626Z</creation></dates><accession>S-EPMC10904683</accession><cross_references><pubmed>38433839</pubmed><doi>10.3389/fimmu.2024.1326354</doi></cross_references></HashMap>