The Experts below are selected from a list of 237 Experts worldwide ranked by ideXlab platform
E De Clercq - One of the best experts on this subject based on the ideXlab platform.
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metabolism of eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a potent inhibitor of inosinate dehydrogenase
Advances in Experimental Medicine and Biology, 1998Co-Authors: Jan Balzarini, L Stet, Akira Matsuda, Leonard I Wiebe, E Knauss, E De ClercqAbstract:The Cytostatic Agent 5-ethynyl-l-β-D-ribofuranosylimidazole-4-carboxamide (EICAR) causes a rapid and marked inhibition of inosinate (IMP) dehydrogenase activity in intact tumor cells. [3H]EICAR is metabolised in L1210 cells to its 5′-mono-, 5′-di- and 5′-triphos-phate in a concentration-dependent manner. The metabolites accumulate proportionally with the initial extracellular EICAR concentrations (ranging from 0.25 to 200 μM). The nicoti-namide adenine dinucleotide (NAD) analogue of EICAR, designated EAD, also accumulates within the cells and becomes the major metabolite after 48 hr incubation with 5 μM [3H]EI-CAR. EAD has a markedly longer intracellular half-life than EICAR 5′-mono-, 5′-di- and 5′-triphosphate. An additional EICAR metabolite elutes on an anion exchange Partisphere SAXHPLC chromatogram between EICAR 5′-di- and 5′-triphosphate. Its intracellular levels are~10-fold lower than those of EAD and the nature of this metabolite has still to be identified. The differential role of EAD and EICAR 5′-monophosphate in the inhibition of IMP dehydrogenase is currently under investigation.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of inosinate dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (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.
Jan Balzarini - One of the best experts on this subject based on the ideXlab platform.
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metabolism of eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a potent inhibitor of inosinate dehydrogenase
Advances in Experimental Medicine and Biology, 1998Co-Authors: Jan Balzarini, L Stet, Akira Matsuda, Leonard I Wiebe, E Knauss, E De ClercqAbstract:The Cytostatic Agent 5-ethynyl-l-β-D-ribofuranosylimidazole-4-carboxamide (EICAR) causes a rapid and marked inhibition of inosinate (IMP) dehydrogenase activity in intact tumor cells. [3H]EICAR is metabolised in L1210 cells to its 5′-mono-, 5′-di- and 5′-triphos-phate in a concentration-dependent manner. The metabolites accumulate proportionally with the initial extracellular EICAR concentrations (ranging from 0.25 to 200 μM). The nicoti-namide adenine dinucleotide (NAD) analogue of EICAR, designated EAD, also accumulates within the cells and becomes the major metabolite after 48 hr incubation with 5 μM [3H]EI-CAR. EAD has a markedly longer intracellular half-life than EICAR 5′-mono-, 5′-di- and 5′-triphosphate. An additional EICAR metabolite elutes on an anion exchange Partisphere SAXHPLC chromatogram between EICAR 5′-di- and 5′-triphosphate. Its intracellular levels are~10-fold lower than those of EAD and the nature of this metabolite has still to be identified. The differential role of EAD and EICAR 5′-monophosphate in the inhibition of IMP dehydrogenase is currently under investigation.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of inosinate dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (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.
Michael Baßler - One of the best experts on this subject based on the ideXlab platform.
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Equilibrium transport velocity of deformable cells and rigid spheres in micro-channels under laminar flow conditions
Microfluidics and Nanofluidics, 2019Co-Authors: Nike Heinß, Sabine Alebrand, Jörn Wittek, Michael BaßlerAbstract:Inertial migration of particles to a characteristic lateral equilibrium position in laminar micro-flows has been investigated under various aspects during the last decades. The majority of the studies deal with the equilibrium position of rigid particles and viscous droplets. Here, we compare the equilibrium velocity of viscoelastic cells and rigid polystyrene spheres in flow by applying the method of spatially modulated emission. The technique allows the precise determination of the equilibrium velocity of an object in flow, which has been found to depend on object characteristics like size in earlier studies. Here, we first show that the deformable cells move at higher equilibrium velocity than rigid polystyrene particles, thus revealing that a particle’s equilibrium velocity is related to its deformability—in addition to size. In a second set of experiments, we treat cells with the Cytostatic Agent colchicine, which results in a systematic decrease of the equilibrium velocity that is attributed to cell stiffening. This study thus provides evidence that the parameter cell deformability can be extracted from the equilibrium velocity based on spatially modulated emission, which opens up an alternative way for high-throughput cell-deformability characterization.
Nike Heinß - One of the best experts on this subject based on the ideXlab platform.
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Equilibrium transport velocity of deformable cells and rigid spheres in micro-channels under laminar flow conditions
Microfluidics and Nanofluidics, 2019Co-Authors: Nike Heinß, Sabine Alebrand, Jörn Wittek, Michael BaßlerAbstract:Inertial migration of particles to a characteristic lateral equilibrium position in laminar micro-flows has been investigated under various aspects during the last decades. The majority of the studies deal with the equilibrium position of rigid particles and viscous droplets. Here, we compare the equilibrium velocity of viscoelastic cells and rigid polystyrene spheres in flow by applying the method of spatially modulated emission. The technique allows the precise determination of the equilibrium velocity of an object in flow, which has been found to depend on object characteristics like size in earlier studies. Here, we first show that the deformable cells move at higher equilibrium velocity than rigid polystyrene particles, thus revealing that a particle’s equilibrium velocity is related to its deformability—in addition to size. In a second set of experiments, we treat cells with the Cytostatic Agent colchicine, which results in a systematic decrease of the equilibrium velocity that is attributed to cell stiffening. This study thus provides evidence that the parameter cell deformability can be extracted from the equilibrium velocity based on spatially modulated emission, which opens up an alternative way for high-throughput cell-deformability characterization.
Litzong Chen - One of the best experts on this subject based on the ideXlab platform.
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alpha fetoprotein response in advanced hepatocellular carcinoma receiving Cytostatic Agent
Journal of Clinical Oncology, 2009Co-Authors: Litzong Chen, Her Shyong Shiah, Yee Chao, Jang Yang Chang, Li Ting Cheng, Jacqueline WhangpengAbstract:TO THEEDITOR:WereadwithinterestthearticlebyChanetal 1 in which they showed that -fetoprotein (AFP) response is an independent prognostic factor for overall survival in patients with advanced hepatocellular carcinoma (HCC) receiving systemic doxorubicinbased chemotherapy. Chan et al also suggested the incorporation of AFP response into the criteria evaluating treatment outcome of advanced HCC in clinical practice and future clinical trials. We had reached similar conclusions based on a study in HCC patients receiv
