Teaching pathology in the 21st century. An experimental automated curriculum delivery system for basic pathology.

In late 1984, the "General Professional Education of the Physician" (GPEP) report recommended, among other things, that medical curricula be revised to rely less on lectures and more on independent study and problem solving. We seem to have anticipated, in 1980, the findings of the GPEP panel by formulating and starting to test the hypothesis that certain "core" information in medical curricula can be as effectively delivered by technology-based self-study means as by lecture or formal laboratory. We began, at that time, to prepare a series of self-study materials using, at first, videotape and then computer-controlled optical videodiscs. The content area selected for study was basic microscopic pathology. The series was planned to cover the following areas of study: cellular alterations and adaptations, cell injury, acute inflammation, chronic inflammation and wound healing, cellular accumulations, circulatory disturbances, necrosis, and neoplasia. All are intended to provide learning experiences in basic pathology. The first two programs were released for testing in 1983 as a two-sided videodisc accompanied by computer-driven pretests, study modules, and posttests that used Apple computers and Pioneer (DiscoVision) videodisc players. An MS DOS (eg, IBM) version of the computer programs was released in 1984. The first two programs are now used in 57 US, Canadian, European, and Philippine health professions schools, and over 1300 student and faculty evaluations have been received. Student and faculty evaluations of these first two programs were very positive, and, as a result, the others are in production and will be completed in 1988. Only when a critical mass of curriculum is available can we really test our stated hypothesis. In the meantime, it is worthwhile to report the evaluation of the first two programs.

Use of the interactive videodisc to teach pathology: a preliminary report.

Although use of computers in education dates to the early 1960s,1-3 it is only with the arrival of the "microcomputer revolution" that computers have become economically feasible in medical education. The advent of inexpensive and relatively powerful microcomputers initiated something of a chain reaction; microcomputers became available for educational purposes, thus creating a market for educational software. This accelerated development of educational software in turn made microcomputers more useable. While synergistic hardware and software development has occurred repeatedly in the microcomputer industry, it is only in the beginning stages in medical education. This paper presents a discussion of the development of one computer-assisted instructional program that utilizes an interactive videodisc format.

Microscopic analysis of early histopathological spinal cord alterations following trauma in normal and cathecholamine-depleted cats.

The progressive histopathological sequence over the first 3 hr after a 400 g-cm blunt injury to the spinal cord of catecholamine (CA)-intact and CA-depleted cats is described. Norepinephrine levels were measured in all animals. The experiments were designed to determine the role of CA in progressive hemorrhagic necrosis of the spinal cord by removing CA from one group of animals prior to trauma. A second group of CA-intact animals was subjected to identical experimentally-induced trauma. Upon analysis of the histopathological changes, it appears that the sequential nature of the development of hemorrhagic necrosis is both qualitatively and quantitatively similar in both experimental groups. The general conclusion is drawn that catecholamines in greater than normal amounts are present at the lesion site after trauma, but these catecholamines are probably not involved in the process of central hemorrhagic necrosis.

Norepinephrine levels in traumatized spinal cord of catecholamine-depleted cats.

This study was designed to elucidate the origin of norepinephrine (NE) measured in spinal cord following trauma. In normal cats the NE concentration at the lesion site increased 63% over control 1 h following experimentally produced blunt trauma (400 g-cm). Spinal cords of adrenalectomized cats were also traumatized, but there was no increase in NE levels 1 h post-trauma. Spinal cord NE levels in these animals were not significantly different from normal or adrenalectomized non-injured controls. In the absence of one of the major peripheral sources of catecholamine, the adrenal medulla, our decreased NE levels prompt us to disagree with the hypothesis that NE measured in injured spinal cord is liberated from intrinsic neuronal systems. It is likely that the mechanism of NE accumulation is directly related to increased circulating levels of NE. The authors speculate on a possible reason for the conflicting results obtained by different laboratories in this area of research.

Mechanical transduction in the Golgi tendon organ: a hypothesis.

Morphological evidence, gained from light and electron microscopy, has shown that the unmyelinated terminal branches of the Ib afferent fiber innervating the Golgi tendon organ (GTO) lie within the spaces between braids of collagen. Based on empirical data it is proposed that force applied to a muscle's tendon will straighten these collagen braids and cause compressional deformation of the axon branches trapped between them. The mechanical events, which are presumed to occur within the GTO, appear to explain how it may function as a biological force transducer under static loading conditions. The mechanical principal described for the GTO may be a primitive and wide-spread biological mechanism employed by certain types of sensory receptors that function as position (and force) detectors.