Co-teaching: a faculty development strategy.

It has been stated that faculty development programmes which are closely linked to particular teaching contexts are most likely to be effective. Over the past 10 years we have developed a model of 'co-teaching' for faculty development which is based upon this premise and which can be applied to any clinical rotation. In this paper we describe our model, in which paired physicians focus on developing their teaching skills while sharing the clinical supervision of residents and medical students. Through iterative phases of teaching, debriefing and planning, co-teachers gain experience in analysing teaching encounters and develop skills in self-evaluation. Teaching occurs in the usual clinical settings such as attending (consultant) teaching rounds, clinic precepting, and case conferences. We discuss our model in the context of educational theory and related literature. We support our positive assessment of the co-teaching model through the precepts of collaborative inquiry and case study methodology. Vignettes, taken from the experiences of the authors, are used to demonstrate how the model is used to develop effective solutions to problems and to help in the maturation of one's skill as an educator. Successful implementation of the model is predicated on the development of a truly collaborative process between co-teachers. We share lessons we have learned from our experience of implementing the model in different clinical venues, such as the contrast between teaching on a hospital ward or in the clinic. This collaborative process has been well received by junior and senior faculty participants in our institution for more than a decade.

Aspirin sensitivity. A distressing reaction that is now often treatable.

Aspirin-induced hypersensitivity affects a substantial number of people, including 20% or more of asthmatic patients. A dramatic flare of symptoms occurs after indigestion of aspirin or a nonsteroidal anti-inflammatory drug, and symptoms can persist even after the agent is discontinued. Fortunately, aspirin desensitization, as described by the authors, now appears to be a treatment option.

In vivo activated T lymphocytes in the peripheral blood and cerebrospinal fluid of patients with multiple sclerosis.

We found an increase in peripheral-blood lymphocytes bearing the T-cell-specific activation antigen Ta1 in 20 of 35 patients with progressive multiple sclerosis, 4 of 18 patients with stable or improving multiple sclerosis, 1 of 17 patients with other neurologic diseases, and 1 of 14 normal controls (P less than 0.0002, Fisher's exact test). No increases in two other markers of T-cell activation, T113 and the interleukin-2 receptor, were found. In the cerebrospinal fluid, patients with progressive multiple sclerosis (pleocytosis, 3.9 +/- 1.6 cells per cubic millimeter) had 42 +/- 3.0 per cent Ta1+ cells. In contrast, patients with other inflammatory central nervous system diseases (36 +/- 13 cells per cubic millimeter) had 9.6 +/- 1.8 per cent Ta1+ cells (P less than 0.01). In patients with other neurologic diseases without inflammation (0.7 +/- 0.16 cells per cubic millimeter), the percentage of Ta1+ cells was equivalent to that in patients with multiple sclerosis (39 +/- 5.4 per cent), although the absolute number was lower. There was a positive correlation between the presence of Ta1+ cells in the spinal fluid and blood of patients with other neurologic diseases, but not patients with multiple sclerosis. Less than 1 per cent of lymphocytes from the spinal fluid of patients with multiple sclerosis expressed interleukin-2 receptors, as compared with 9.8 per cent of cells from subjects with other inflammatory neurologic diseases (P less than 0.01). These results suggest that the T cells in the spinal fluid of patients with multiple sclerosis may be activated by a different mechanism or in a different temporal sequence from that in patients with other nervous system diseases. Furthermore, the increase in Ta1+ cells in the peripheral blood of patients with multiple sclerosis demonstrates systemic immune activation in the disease; monitoring such cells may provide an objective measure of abnormal immunologic activity.