Use of bar coding technology to flag ER patients on metformin-containing drugs.

Sixty percent of Jennie Edmundson Hospital's inpatients are admitted through the emergency room. Type II diabetes accounts for 90-95% of all diagnosed cases of diabetes. There were about 1.6 million new cases of diabetes diagnosed in people 20 years or older in 2007. Consequently, we should expect to see an increase in Americans on metformin-containing drugs in the future. Jennie Edmundson Hospital's goal was to develop a hardwired process to identify patients on the medication metformin and who had a CT scan with contrast in the ER and were then admitted as an inpatient.

Maintenance of cellular respiration indicates drug resistance in acute myeloid leukemia.

Primary resistance to induction therapy is an unsolved clinical problem in acute myeloid leukemia (AML). Here we investigated drug resistance in AML at the level of cellular metabolism in order to identify early predictors of therapeutic response. Using extracellular flux analysis, we compared metabolic drug responses in AML cell lines sensitive or resistant to cytarabine or sorafenib after 24h of drug treatment to a small cell lung cancer (SCLC) cell line exposed to etoposide. Only drug-resistant AML cells maintained oxidative metabolism upon drug exposure while SCLC cells displayed an overall metabolic shift towards glycolysis, i.e. a Warburg effect to escape drug toxicity. Moreover, primary AML blasts displayed very low glycolytic activity, while oxygen consumption was readily detectable, indicating an essential role of oxidative pathways in the bioenergetics of AML blasts. In line with these observations, analysis of the mitochondrial membrane potential using tetramethylrhodamine ethyl ester staining and flow cytometry allowed for clear discrimination between drug sensitive and resistant AML cell line clones and primary blasts after 24h of treatment with cytarabine or sorafenib. Our data reveal a distinct metabolic phenotype of resistant AML cells and suggest that disrupting oxidative metabolism rather than glycolysis may enhance the cytotoxic effects of chemotherapy in AML.