Project description:Focal cortical dysplasia (FCD), a focal brain malformation, is the most common cause of intractable epilepsy. One of the related disorders is tuberous sclerosis (TS). The dysplasia appears to result from a defect in cortical development, however, this disorder is heterogeneous, and FCD seizure therapy is non-specific and failure-prone. As a final recourse, patients may undergo multiple surgical resections to control seizures. Thus, there is a clinical need to characterize this disorder with respect to structural, molecular, and electrophysiological profiles, which will lead to development of animal models and pilot therapies that we will then apply to humans.
Project description:Focal Cortical Dysplasia (FCD) is a major cause of drug-resistant focal epilepsy in children and the clinico-pathological classification remains a challenging issue in daily practice. With the recent progress in DNA methylation based classification of human brain tumors we examined, whether genomic DNA methylation and gene expression analysis can be used to also distinguish human FCD subtype
Project description:Focal Cortical Dysplasia (FCD) is a major cause of drug-resistant focal epilepsy in children and the clinico-pathological classification remains a challenging issue in daily practice. With the recent progress in DNA methylation based classification of human brain tumors we examined, whether genomic DNA methylation and gene expression analysis can be used to also distinguish human FCD subtype
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
