<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/GSE345nnn/GSE345466/</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=GSE345466</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Developmental Arrest Associated with Altered Cerebellar Metabolism in Sudden Infant Death Syndrome</name><description>Sudden infant death syndrome (SIDS) may involve impaired cerebellar contributions to autonomic and arousal responses during hypoxic stress. We performed bulk RNA sequencing of flash-frozen postmortem human cerebellar cortex from SIDS infants and age-matched non-SIDS controls to define transcriptional alterations associated with SIDS. Differential-expression and pathway-enrichment analyses were used to evaluate neuroinflammatory, neurotransmitter, and metabolic programs, and transcriptomic findings were compared at the pathway level with independently generated targeted metabolomics and quantitative histology data.</description><dates><publication>2026/08/30</publication></dates><accession>GSE345466</accession><cross_references><GSM>GSM10005134</GSM><GSM>GSM10005145</GSM><GSM>GSM10005144</GSM><GSM>GSM10005133</GSM><GSM>GSM10005136</GSM><GSM>GSM10005135</GSM><GSM>GSM10005146</GSM><GSM>GSM10005141</GSM><GSM>GSM10005130</GSM><GSM>GSM10005140</GSM><GSM>GSM10005132</GSM><GSM>GSM10005143</GSM><GSM>GSM10005142</GSM><GSM>GSM10005131</GSM><GSM>GSM10005138</GSM><GSM>GSM10005137</GSM><GSM>GSM10005129</GSM><GSM>GSM10005139</GSM><GPL>24676</GPL><GSE>345466</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>