human
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['Atrial fibrillation (AF) is a progressive disease. Previously, clinical and animal experimental studies in AF revealed a variety of myocyte remodeling processes including L-type Ca(2+) channel reduction and structural changes, which finally result in electrical remodeling and contractile dysfunction. There are indications that myocyte remodeling is mediated by Ca(2+) overload induced calpain activation. To study in more detail the mechanisms underlying myocyte remodeling and to develop strategies for drug-interference, we utilised a paced cell model for AF.', 'HL-1 atrial myocytes were subjected to a 10 times increase in rate over basal values by electrical field stimulation at 5 Hz. It was found that 24-h pacing reduced plasmalemmal levels of L-type Ca(2+) channel alpha 1C subunit by -72% compared to controls. No changes in amount of the potassium channel subunits Kv4.3 and Kv1.5 were found. Pacing also induced marked structural changes; myolysis and nuclear condensation, paralleled by a 14-fold increase in calpain activity. The pacing-induced reduction of L-type Ca(2+) channel protein was fully prevented by treatment with verapamil, the active stereoisomer of methoxyverapamil D600, the calpain inhibitors PD150606 and E64d, and LaCl(3). Interestingly, PD150606, E64d and LaCl(3), but not (methoxy)verapamil, prevented structural changes.'] Does calpain inhibition prevent pacing-induced cellular remodeling in a HL-1 myocyte model for atrial fibrillation?
OUTPUT:

agent
yes
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['Atrial fibrillation (AF) is a progressive disease. Previously, clinical and animal experimental studies in AF revealed a variety of myocyte remodeling processes including L-type Ca(2+) channel reduction and structural changes, which finally result in electrical remodeling and contractile dysfunction. There are indications that myocyte remodeling is mediated by Ca(2+) overload induced calpain activation. To study in more detail the mechanisms underlying myocyte remodeling and to develop strategies for drug-interference, we utilised a paced cell model for AF.', 'HL-1 atrial myocytes were subjected to a 10 times increase in rate over basal values by electrical field stimulation at 5 Hz. It was found that 24-h pacing reduced plasmalemmal levels of L-type Ca(2+) channel alpha 1C subunit by -72% compared to controls. No changes in amount of the potassium channel subunits Kv4.3 and Kv1.5 were found. Pacing also induced marked structural changes; myolysis and nuclear condensation, paralleled by a 14-fold increase in calpain activity. The pacing-induced reduction of L-type Ca(2+) channel protein was fully prevented by treatment with verapamil, the active stereoisomer of methoxyverapamil D600, the calpain inhibitors PD150606 and E64d, and LaCl(3). Interestingly, PD150606, E64d and LaCl(3), but not (methoxy)verapamil, prevented structural changes.'] Does calpain inhibition prevent pacing-induced cellular remodeling in a HL-1 myocyte model for atrial fibrillation?
OUTPUT:
