Science and Engineering Ethics Education: Recipes for Success

This presentation was part of the AAAS Annual Conference professional development workshop, National Science Foundation and Ethics Education in Science and Engineering, during the recent meeting in San Diego, California (18-22 February). Dr. Michael Gorman, Program Director, Science, Technology & Society, National Science Foundation, moderated the workshop presentations and the discussion that followed. In addition, he contributed a set of powerpoint slides outlining the role of NSF in its response to the America Competes Act, including a commitment to support an online resource in ethics education. Dr. Philip Langlais, Vice Provost for Graduate Studies & Research, Old Dominion University, presented recommendations for developing institutional RCR and mentoring programs based on the new NSF and NIH RCR requirements. Dr. Kathleen Flint, Project Manager, National Postdoctoral Association, gave recommendations for unique RCR training needs of postdocs and reported on the NPA Bring RCR Home Project, a national project that worked to develop local RCR programs for postdocs. Dr. Jane Fountain, Professor of Political Science and Public Policy, and Director of the National Center for Digital Government and the Science, Technology & Society Initiative, University of Massachusetts Amherst, presented recent developments at ESENCe, one of the beta sites sponsored by NSF. The purpose of ESENCe is to preserve and widely disseminate a variety of materials on ethics and the responsible conduct of research in science and engineering disciplines. In addition, the presentation summarized recent development of cases, background notes and teaching materials regarding international dimensions of ethics education

A corticosteroid/dopamine hypothesis for psychotic depression and related states

In recent years, considerable data have emerged that psychotic (delusional) depression is characterized by pronounced increases in hypothalamic-pituitary-adrenal (HPA) axis activity and positive responses to combined treatment with tricyclic antidepressants and antipsychotic (dopamine-blocking) agents. Recently, a number of observations in several species, including man, point to glucocorticoids\u27 increasing dopamine activity in a variety of tissues and this effect is particularly marked in rat brain mesolimbic dopamine systems. We propose that glucocorticoids\u27 enhancement of dopaminergic activity may explain the development of psychosis/delusions in the context of the depressive episode. Data in support of the hypothesis are presented and the identification of possible enzymatic risk factors are discussed. These interactions also have implications for understanding the biology of corticosteroid-induced psychoses in medical patients and some of the psychiatric complications of Cushing\u27s Disease

Psychotic and nonpsychotic depressions: II. Platelet MAO activity, plasma catecholamines, cortisol, and specific symptoms

Preliminary data are presented on levels of plasma cortisol, dopamine (DA), epinephrine (EPI), and norepinephrine (NE) before and after dexamethasone in 22 depressed patients (of whom 4 were psychotic). Platelet monoamine oxidase (MAO) activity, determined in 19 of the depressed patients, was significantly higher in the 4 psychotic patients than it was in the 15 nonpsychotic patients. Positive correlations were observed before and after dexamethasone among cortisol, DA, EPI, and platelet MAO. After dexamethasone, plasma NE correlated negatively with DA, EPI, and cortisol. The various correlations were due largely to the inclusion of the psychotic depressive subgroup. Data are also presented on the relationships between these biological measures and specific signs and symptoms

Psychotic and nonpsychotic depressions: I. comparisons of plasma catecholamines and cortisol measures

Unconjugated plasma catecholamines and cortisol were measured before and after a 1 mg dose of dexamethasone in 22 medication-free depressed patients and 6 healthy, medication-free control subjects. Plasma dopamine (DA) levels in the psychotically depressed subgroup (n=4) were significantly higher both before and after dexamethasone than those in the nonpsychotic depressed group and higher before dexamethasone than in the control group. Similarly, the psychotically depressed group exhibited significantly higher cortisol levels both before and after dexamethasone than the nonpsychotic depressed group or the control group. In contrast, the psychotically depressed group had significantly lower postdexamethasone plasma norepinephrine levels compared to the nonpsychotic depressed group. In both patients and controls, plasma DA was significantly higher after dexamethasome administration than before, but the magnitude of the increase was 10 times greater in controls than in patients. © 1987

Dexamethasone increases plasma free dopamine in man

In man, unconjugated plasma DA is normally undetectable or present in minute amounts. Twelve medication-free volunteers received a 1 mg dose of dexamethasone which produced pronounced increases of plasma free DA but not of other catecholamines. Mean plasma free dopamine levels after dexamethasone at 8 a.m. (155 +/- 102 pg/ml) and 4 p.m. (163 +/- 70 pg/ml) were significantly higher (p less than 0.001) than those at 8 a.m. (50 +/- 18 pg/ml) and 4 p.m. (42 +/- 7 pg/ml) before dexamethasone. Although the mechanism of increased dopaminergic activity after a dose of dexamethasone remains for future research, the data presented in this paper may explain the observations that corticosteroids lower prolactin levels and may induce psychiatric disturbances, as well as the finding that depressed patients with high postdexamethasone cortisol levels are frequently psychotic

The effects of a single acute dose of dexamethasone on monoamine and metabolite levels in rat brain

Twenty male Sprague-Dawley rats were injected intraperitoneally with either 20 μg. of dexamethasone or an equivalent volume of saline. The rats were then sacrificed at either one or four hours after the injections and their brains analyzed for monoamine and metabolite content using High Performance Liquid Chromatography with Electrochemical Detection. Significant effects were seen in dopaminergic and serotonergic systems, but these effects varied depending on the area of rat brain studied. Significant increases in dopamine (DA) levels were seen in the hypothalamus and nucleus accumbens of the dexamethasone treated rats when compared with saline treated rats. There was no significant effect of dexamethasone on DA levels in frontal or striatal brain areas. In the dexamethasone treated rats a significant increase in serotonin (5-HT) was observed in the hypothalamus; a significant decrease in 5-HT was observed in the frontal cortex. Biological and clinical implications of these findings are discussed. © 1985