human
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['Many local anaesthetics are non-competitive inhibitors of nicotinic receptors (acetylcholine receptor, AChR). Proadifen induces a high-affinity state of the receptor, but its mechanism of action and that of an analogue, adiphenine, is unknown.', 'We measured the effects of proadifen and adiphenine on single-channel and macroscopic currents of adult mouse muscle AChR (wild-type and mutant). We assessed the results in terms of mechanisms and sites of action.', 'Both proadifen and adiphenine decreased the frequency of ACh-induced single-channel currents. Proadifen did not change cluster properties, but adiphenine decreased cluster duration (36-fold at 100 micromolxL(-1)). Preincubation with proadifen decreased the amplitude (IC(50)= 19 micromolxL(-1)) without changing the decay rate of macroscopic currents. In contrast, adiphenine did not change amplitude but increased the decay rate (IC(50)= 15 micromolxL(-1)). Kinetic measurements demonstrate that proadifen acts on the resting state to induce a desensitized state whose kinetics of recovery resemble those of ACh-induced desensitization. Adiphenine accelerates desensitization from the open state, but previous application of the drug to resting receptors is required. Both drugs stabilize desensitized states, as evidenced by the decrease in the number of clusters elicited by high ACh concentrations. The inhibition by adiphenine is not affected by proadifen, and the mutation alphaE262K decreases the sensitivity of the AChR only for adiphenine, indicating that these drugs act at different sites.'] Do the local anaesthetics proadifen and adiphenine inhibit nicotinic receptors by different molecular mechanisms?
OUTPUT:

agent
yes
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['Many local anaesthetics are non-competitive inhibitors of nicotinic receptors (acetylcholine receptor, AChR). Proadifen induces a high-affinity state of the receptor, but its mechanism of action and that of an analogue, adiphenine, is unknown.', 'We measured the effects of proadifen and adiphenine on single-channel and macroscopic currents of adult mouse muscle AChR (wild-type and mutant). We assessed the results in terms of mechanisms and sites of action.', 'Both proadifen and adiphenine decreased the frequency of ACh-induced single-channel currents. Proadifen did not change cluster properties, but adiphenine decreased cluster duration (36-fold at 100 micromolxL(-1)). Preincubation with proadifen decreased the amplitude (IC(50)= 19 micromolxL(-1)) without changing the decay rate of macroscopic currents. In contrast, adiphenine did not change amplitude but increased the decay rate (IC(50)= 15 micromolxL(-1)). Kinetic measurements demonstrate that proadifen acts on the resting state to induce a desensitized state whose kinetics of recovery resemble those of ACh-induced desensitization. Adiphenine accelerates desensitization from the open state, but previous application of the drug to resting receptors is required. Both drugs stabilize desensitized states, as evidenced by the decrease in the number of clusters elicited by high ACh concentrations. The inhibition by adiphenine is not affected by proadifen, and the mutation alphaE262K decreases the sensitivity of the AChR only for adiphenine, indicating that these drugs act at different sites.'] Do the local anaesthetics proadifen and adiphenine inhibit nicotinic receptors by different molecular mechanisms?
OUTPUT:
