Advanced Technology Training System on Motor-Operated Valves

This paper describes how features from the field of Intelligent Tutoring Systems are applied to the Motor-Operated Valve (MOV) Advanced Technology Training System (ATTS). The MOV ATTS is a training system developed at Galaxy Scientific Corporation for the Central Research Institute of Electric Power Industry in Japan and the Electric Power Research Institute in the United States. The MOV ATTS combines traditional computer-based training approaches with system simulation, integrated expert systems, and student and expert modeling. The primary goal of the MOV ATTS is to reduce human errors that occur during MOV overhaul and repair. The MOV ATTS addresses this goal by providing basic operational information of the MOV, simulating MOV operation, providing troubleshooting practice of MOV failures, and tailoring this training to the needs of each individual student. The MOV ATTS integrates multiple expert models (functional and procedural) to provide advice and feedback to students. The integration also provides expert model validation support to developers. Student modeling is supported by two separate student models: one model registers and updates the student's current knowledge of basic MOV information, while another model logs the student's actions and errors during troubleshooting exercises. These two models are used to provide tailored feedback to the student during the MOV course

Nicotinic acetylcholine receptor-mediated neuroprotection by donepezil against glutamate neurotoxicity in rat cortical neurons. J Pharmacol Exp Ther 306: 772–777

ABSTRACT Donepezil is a potent and selective acetylcholinesterase (AChE) inhibitor developed for the treatment of Alzheimer's disease. To elucidate whether donepezil shows neuroprotective action in addition to amelioration of cognitive deficits, we examined the effects of donepezil on glutamate-induced neurotoxicity using primary cultures of rat cortical neurons. A 10-min exposure of cultures to glutamate followed by a 1-h incubation with glutamatefree medium caused a marked loss of viability, as determined by Trypan blue exclusion. Glutamate neurotoxicity was prevented by 24-h pretreatment of donepezil in a concentration-dependent manner. Among AChE inhibitors examined, donepezil and certain AChE inhibitors such as tacrine and galanthamine showed potent neuroprotective action, although physostigmine did not affect glutamate neurotoxicity. Neuroprotective action of donepezil was antagonized by mecamylamine, a nicotinic acetylcholine receptor (nAChR) antagonist, but not by scopolamine, a muscarinic acetylcholine receptor antagonist. Furthermore, both dihydro-␤-erythroidine, an ␣4␤2-neuronal nAChR antagonist, and methyllycaconitine, an ␣7-nAChR antagonist, each also significantly antagonized the effect of donepezil. Next, we examined the effects of donepezil on glutamate-induced apoptosis. Exposure of 100 M glutamate to cortical neurons for 24 h induced apoptotic neuronal death and nuclear fragmentation. Donepezil for 24 h before and 24 h during glutamate exposure prevented nuclear fragmentation and glutamate-induced apoptosis. These results suggest that donepezil not only protects cortical neurons against glutamate neurotoxicity via ␣4␤2-and ␣7-nAChRs but also prevents apoptotic neuronal death