The authors raise questions regarding the wide-spread calls emanating from lay and medical audiences alike to intensify the formal teaching of ethics within the medical school curriculum. In particular, they challenge a prevailing belief within the culture of medicine that while it may be possible to teach information about ethics (e.g., skills in recognizing the presence of common ethical problems, skills in ethical reasoning, or improved understanding of the language and concepts of ethics), course material or even an entire curriculum can in no way decisively influence a student's personality or ensure ethical conduct. To this end, several issues are explored, including whether medical ethics is best framed as a body of knowledge and skills or as part of one's professional identity. The authors argue that most of the critical determinants of physician identity operate not within the formal curriculum but in a more subtle, less officially recognized "hidden curriculum." The overall process of medical education is presented as a form of moral training of which formal instruction in ethics constitutes only one small piece. Finally, the authors maintain that any attempt to develop a comprehensive ethics curriculum must acknowledge the broader cultural milieu within which that curriculum must function. In conclusion, they offer recommendations on how an ethics curriculum might be more fruitfully structured to become a seamless part of the training process.

The sensory disturbance in schizophrenia is often described as an inability to filter out extraneous noise from meaningful sensory inputs. The neurobiological basis of this inability to filter has been examined using auditory evoked potentials, which are computerized averages of the brain's electrical response to sound. The sounds are presented in pairs to test the ability of the brain to inhibit, or gate, its response to a repeated stimulus. Schizophrenic patients lack the ability to gate the neuronal response shown by a particular wave, the P50 wave. The measurement of this deficit in human subjects and the exploration of its neurobiology in animals has produced evidence about several issues in the pathophysiology of schizophrenia: (1) the role of dopamine in improvement of sensory function in schizophrenic patients treated with neuroleptic drugs, (2) the interaction between familial or genetic deficits in sensory functioning in schizophrenic patients and possible abnormalities in dopamine metabolism, and (3) a mechanism by which noradrenergic hyperactivity in mania and other psychiatric illnesses might mimic some pathophysiological deficits in schizophrenia.

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