There was no correlation between corrected absolute FMZ-Vd and HCV or neuronal cell density. After partial-volume effects correction all 17 patients (100%) showed both significant unilateral reduction of absolute FMZ-Vd and abnormal FMZ-AI. Absolute FMZ-Vd and asymmetry indices (FMZ-AI) were compared before and after partial-volume effect correction with MRI-determined hippocampal volumes (HCV), hippocampal T2 measurements, and, if available, neuronal cell densities.Ĭompared with 15 age-matched healthy volunteers, significant reductions of absolute hippocampal FMZ-Vd were found before correction for partial-volume effects in 11 of 17 patients (65%) and only abnormal FMZ-AI in the other six patients. Quantitative neuropathology was performed with assessment of neuron density in 14 of the 17 patients. We determined hippocampal volume loss and reduction in cBZR binding using an MRI-based method for partial-volume effect correction of 11C-FMZ volume of distribution (FMZ-Vd) in 17 patients with refractory mTLE and an MRI diagnosis of HS that was subsequently histologically verified in all cases. The limited spatial resolution of PET, however, results in partial-volume averaging that affects quantitative analysis of cBZR density. ![]() This work can lead to new insights for the management of disease states.Using statistical parametric mapping and 11C-flumazenil (FMZ) PET we have previously shown reduction of central benzodiazepine receptor (cBZR) binding restricted to the hippocampus in mesial temporal lobe epilepsy (mTLE) due to hippocampal sclerosis (HS). Studies demonstrate that chromosomes move and interconnect within a cell in response to cell-cell and environmental signaling from nutrients and the human microbiome. Now, researchers are beginning to understand that cells have dynamic microenvironments. Applying this understanding to clinical decision making improves patient care. The human genome may harbor genes with mutations and variations that impact disease susceptibility and therapeutic responses. Cunningham and her colleagues have carried out genomic and epigenomic analyses, yielding distinctions between the different histology subtypes. This disease has a high rate of mortality due to the paucity of symptoms in the early stages of the disease. Cunningham's research is ongoing in this area. Sequencing of DNA and RNA have yielded differences between controls, who have benign breast disease without cancer, and people who go on to develop subsequent cancers. Cunningham and her colleagues is on understanding whether an outcome can be predicted. This condition confers a risk of developing breast cancer. This research has implications for the development of therapeutic options. Such defects may result from the inheritance of a defective gene or, in sporadic cases, hypermethylation of a gene. Clinical tests for colorectal cancer incorporate testing for defective DNA mismatch repair. ![]() Cunningham's earlier work focused on hereditary nonpolyposis colorectal cancer and DNA mismatch repair genes. She works closely with individuals from biostatistics, epidemiology, and Mayo Clinic's cancer and genomics centers. Cunningham also participates in research projects involving benign breast disease, and ovarian and colon cancers. As a co-director of the Genome Analysis Core, Dr. Her primary focus is on the genetic mechanisms underlying the development of cancer, including cancers of the colon, prostate, ovary, breast and pancreas, as well as non-Hodgkin's lymphoma and chronic lymphocytic leukemia. ![]() ![]() Cunningham, Ph.D., aims to elucidate of the genetic basis of disease.
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