carbonyl cyanide p-trifluoromethoxyphenylhydrazone has been researched along with dibucaine in 4 studies
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (25.00) | 18.7374 |
| 1990's | 2 (50.00) | 18.2507 |
| 2000's | 1 (25.00) | 29.6817 |
| 2010's | 0 (0.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Cooper, CE; Nicholls, P; Sharpe, MA; Wrigglesworth, JM | 1 |
| Darnold, JR; Fleschner, CR; Long, JW; Martin, AP; Vorbeck, ML | 1 |
| Bernardi, P; Petronilli, V; Veronese, P | 1 |
| Akaike, A; Honda, K; Inoue, R; Kihara, T; Nakamizo, T; Sawada, H; Shimohama, S; Urushitani, M | 1 |
4 other study(ies) available for carbonyl cyanide p-trifluoromethoxyphenylhydrazone and dibucaine
| Article | Year |
|---|---|
The proteoliposomal steady state. Effect of size, capacitance and membrane permeability on cytochrome-oxidase-induced ion gradients.
Topics: Animals; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; Cattle; Cell Membrane; Dibucaine; Electron Transport Complex IV; Hydrogen-Ion Concentration; In Vitro Techniques; Ionophores; Membrane Potentials; Models, Theoretical; Oleic Acid; Oleic Acids; Permeability; Proteolipids; Protons; Valinomycin | 1990 |
Ca2+ release from energetically coupled tumor mitochondria.
Topics: Animals; Calcium; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; Carcinoma, Ehrlich Tumor; Cell Line; Dibucaine; Male; Mice; Mitochondria; Sodium; Trifluoperazine; Verapamil | 1983 |
Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore. I. Evidence for two separate Me2+ binding sites with opposing effects on the pore open probability.
Topics: Animals; Binding Sites; Calcium; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; Cyclosporine; Dibucaine; Egtazic Acid; Hydrogen-Ion Concentration; Intracellular Membranes; Kinetics; Magnesium; Membrane Potentials; Mitochondria, Liver; Permeability; Probability; Rats; Trifluoperazine | 1993 |
N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+) overload in acute excitotoxic motor neuron death: a mechanism distinct from chronic neurotoxicity after Ca(2+) influx.
Topics: 2,4-Dinitrophenol; 6-Cyano-7-nitroquinoxaline-2,3-dione; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Calcium Signaling; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; Cells, Cultured; Cyclosporine; Dibucaine; Dizocilpine Maleate; Enzyme Inhibitors; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Fluoresceins; Fluorescent Dyes; Glutamic Acid; Heterocyclic Compounds, 3-Ring; Imidazoles; Kainic Acid; Mitochondria; Motor Neuron Disease; Motor Neurons; N-Methylaspartate; Nerve Tissue Proteins; Neurons; Neurotoxins; Nitric Oxide Synthase; Nitric Oxide Synthase Type I; Oxidative Stress; Rats; Rats, Wistar; Reactive Oxygen Species; Receptors, AMPA; Receptors, Kainic Acid; Receptors, N-Methyl-D-Aspartate; Rhodamines; Spinal Cord; Superoxide Dismutase; Uncoupling Agents | 2001 |