<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE244nnn/GSE244596/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE244596</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Dysregulated gene expression in human rheumatoid arthritis-associated interstitial lung disease(RA-ILD) and rheumatoid arthritis (RA) peripheral blood samples</name><description>RA-associated interstitial lung disease (RA-ILD) is an increasingly recognized extra-articular manifestations (EAMs) in the RA, with highly morbidity and mortality. Due to the etiology of RA-ILD is unknown, we collected peripheral blood samples of RA-ILD and RA patients. Differential gene expression analysis was employed to identify key genes, common pathways, and potential drug targets for RA-ILD. Furthermore, RT-qPCR was conducted to verify potential biomarkers in RA-ILD.This study was undertaken to understand the disease's molecular basis better and provide relevant insight into phenotypical alterations and mechanisms involved in RA-ILD pathogenesis.</description><dates><publication>2026/10/01</publication></dates><accession>GSE244596</accession><cross_references><GSM>GSM7821525</GSM><GSM>GSM7821533</GSM><GSM>GSM7821534</GSM><GSM>GSM7821531</GSM><GSM>GSM7821532</GSM><GSM>GSM7821530</GSM><GSM>GSM7821528</GSM><GSM>GSM7821529</GSM><GSM>GSM7821526</GSM><GSM>GSM7821527</GSM><GPL>30209</GPL><GSE>244596</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>