37 research outputs found
On Neglecting Chemical Exchange When Correcting in Vivo31P MRS Data for Partial Saturation: Commentary on: “Pitfalls in the Measurement of Metabolite Concentrations Using the One-Pulse Experiment in in Vivo NMR”
No full textCorrectly accounting for radiofrequency spillover in saturation transfer experiments: application to measurement of the creatine kinase reaction rate in human forearm muscle
No full textEICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide). A novel potent inhibitor of inosinate dehydrogenase activity and guanylate biosynthesis
No full textEICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide) is a cytostatic agent that inhibits murine leukemia L1210 and human lymphocyte CEM cells at a 50% inhibitory concentration of 0.80-1.4 microM, respectively. EICAR causes a rapid and marked inhibition of inosinate (IMP) dehydrogenase (EC 1.1.1.205) activity in intact L1210 and CEM cells reflected by a concentration-dependent accumulation of IMP and depletion of GTP and dGTP levels. EICAR 5'-monophosphate is a potent inhibitor of purified L1210 cell IMP dehydrogenase (Ki/Km 0.06). Inhibition of IMP dehydrogenase by EICAR 5'-monophosphate is competitive with respect to IMP. L1210 cells that were selected for resistance to the cytostatic action of EICAR proved to be adenosine kinase-deficient. Also, studies with other mutant L1210 and CEM cell lines revealed that adenosine kinase, as well as an alternative pathway, may be responsible for the conversion of EICAR to its 5'-monophosphate. Purified 2'-deoxycytidine kinase, 2'-deoxyguanosine kinase, cytosolic 5'-nucleotidase, and nicotinamide dinucleotide (NAD) pyrophosphorylase do not seem to be markedly involved in the metabolism of EICAR.status: publishe
On Neglecting Chemical Exchange Effects When Correcting in Vivo31P MRS Data for Partial Saturation
No full textLow Cerebellar Vermis Volumes and Impaired Neuropsychologic Performance in Children Treated for Brain Tumors and Leukemia
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