<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/GSE295nnn/GSE295236/</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=GSE295236</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Excitatory neurons and astrocytes-specific dysregulation and aberrant interactions are vulnerable to FCDI as suggested by single-cell spatial transcriptomics [snRNA-seq]</name><description>Focal cortical dysplasia (FCD) is a common neurodevelopmental disorder characterized by malformations of cortical development and is a leading cause of drug-resistant epilepsy. In this study, we employed single-nucleus RNA sequencing (snRNA-seq) and spatial transcriptomics sequencing (ST-seq) to investigate the molecular pathological features of FCD type I (FCDI) brain tissue from both cell type-specific and spatial heterogeneity perspectives. This integrated analysis provides novel theoretical insights into the pathogenesis of FCDI associated epilepsy.</description><dates><publication>2026/04/21</publication></dates><accession>GSE295236</accession><cross_references><GSM>GSM8944107</GSM><GSM>GSM8944106</GSM><GSM>GSM8944105</GSM><GSM>GSM8944104</GSM><GSM>GSM8944103</GSM><GSM>GSM8944102</GSM><GPL>34284</GPL><GSE>295236</GSE><taxon>Homo sapiens</taxon><PMID>[42068085]</PMID></cross_references></HashMap>