The Impact of Students\u27 Perceived Computer Experience on Behavior and Performance in an Introductory Information Systems Course

In this study the impact of perceived computer experience on the behavior and performance of students in an introductory information systems (IS) course with both lab and lecture components was examined. Perceived computer experience was predicted to affect behavior and performance in the course because of its relationship to positive internal attitudes towards computers and because students\u27 perceptions of their computer experience are related to their actual level of knowledge about computers. The results of the study showed that higher levels of perceived computer experience positively affected lecture and lab homework and exam performance. In addition, higher levels of positive class behaviors (attendance and extra-credit participation) positively affected both lecture and lab exam performance. Gender and lab/lecture section were included as control variables and both had an impact on behavior and performance. Women participated more in extra-credit opportunities. Lecture and lab sections varied significantly with regard to attendance, extra-credit participation, lab homework, and lab and lecture exam performance. These results are discussed in the context of previous research on factors affecting introductory information systems course performance and prior research on the effects of prior computer experience on learning

Dispatcher: A Theory-Based Design for Study of Real-Time Decision-Making

Dispatcher is a computer simulation being used in a series of experiments involving the study of real-time dynamic decision making. The design of the simulation is based on current theory of providing decision support for this type of decision making task. This paper provides an overview of the process used in designing and implementing Dispatcher, as well as a description of some of the main features of the simulation as they relate to current research efforts in the study of decision support for RTDDM

PERFORMANCE =/= BEHAVIOR: A STUDY IN THE FRAGILITY OF EXPERTISE

The fragility of expertise is a known, but little understood, feature of expert reasoning. Essentially, fragili(y refers to the performance degradation of experts as task properties change. A study is presented in which the fragility of expertise in a complex, real-world task -- reactive scheduling -- is investigated. Six novices (students, trained in the task but with no experience in the domain) and three expert schedulers (ranging from six to 20 years of experience in the domain) each completed six reactive scheduling tasks varying in difficulty. All subjects were run individually and their protocols (verbal and action) were recorded on video-tape. Simple modifications to the task environment were sufficient to degrade the pelfonnance of the experts, sometimes to the level of the novices. However, an analysis of the behavior of the subjects suggests that a problem space characterization of fragility can explain how that degradation occurred. The behavior captured in the video-tapes (both verbal utterances and physical actions) show that, in this task, the primary source of degradation was the inappropriate formation of problem space components. That is, experts were stuck in the wrong problem space. Specifically, the experts would use inadequate search control knowledge while traversing problem spaces and/or repeatedly attempt to implement operators or types of search control knowledge that were not allowed in the experimental task, but were quite valid in the real task setting. We conclude by discussing the concept of expert fragility and how it should be taken into account when designing systems based on the construct of expertise: expert systems

Regulation of Thalamic and Cortical Network Synchrony by Scn8a.

Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamocortical circuits leading to non-convulsive absence epilepsy. We found that loss of Scn8a leads to altered RT cell intrinsic excitability and a failure in recurrent RT synaptic inhibition. We propose that these deficits cooperate to enhance thalamocortical network synchrony and generate pathological oscillations. To our knowledge, this finding is the first clear demonstration of a pathological state tied to disruption of the RT-RT synapse. Our observation that loss of a single gene in the thalamus of an adult wild-type animal is sufficient to cause spike-wave discharges is striking and represents an example of absence epilepsy of thalamic origin

Regulation of Thalamic and Cortical Network Synchrony by Scn8a

Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamocortical circuits leading to non-convulsive absence epilepsy. We found that loss of Scn8a leads to altered RT cell intrinsic excitability and a failure in recurrent RT synaptic inhibition. We propose that these deficits cooperate to enhance thalamocortical network synchrony and generate pathological oscillations. To our knowledge, this finding is the first clear demonstration of a pathological state tied to disruption of the RT-RT synapse. Our observation that loss of a single gene in the thalamus of an adult wild-type animal is sufficient to cause spike-wave discharges is striking and represents an example of absence epilepsy of thalamic origin

Regulation of Thalamic and Cortical Network Synchrony by Scn8a.

Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamocortical circuits leading to non-convulsive absence epilepsy. We found that loss of Scn8a leads to altered RT cell intrinsic excitability and a failure in recurrent RT synaptic inhibition. We propose that these deficits cooperate to enhance thalamocortical network synchrony and generate pathological oscillations. To our knowledge, this finding is the first clear demonstration of a pathological state tied to disruption of the RT-RT synapse. Our observation that loss of a single gene in the thalamus of an adult wild-type animal is sufficient to cause spike-wave discharges is striking and represents an example of absence epilepsy of thalamic origin