The effects of three strategies for changing stigmatizing attitudes--education (which replaces myths about mental illness with accurate conceptions), contact (which challenges public attitudes about mental illness through direct interactions with persons who have these disorders), and protest (which seeks to suppress stigmatizing attitudes about mental illness)--were examined on attributions about schizophrenia and other severe mental illnesses. One hundred and fifty-two students at a community college were randomly assigned to one of the three strategies or a control condition. They completed a questionnaire about attributions toward six groups--depression, psychosis, cocaine addiction, mental retardation, cancer, and AIDS--prior to and after completing the assigned condition. As expected, results showed that education had no effect on attributions about physical disabilities but led to improved attributions in all four psychiatric groups. Contact produced positive changes that exceeded education effects in attributions about targeted psychiatric disabilities: depression and psychosis. Protest yielded no significant changes in attributions about any group. This study also examined the effects of these strategies on processing information about mental illness.

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Victims of major electrical trauma frequently suffer extensive skeletal muscle and nerve damage, which is postulated to be principally mediated by electroporation and/or thermally driven cell membrane permeabilization. We have investigated the efficacy oftwo blood-compatible chemical surfactants for sealing electroporated muscle membranes. In studies using cultured skeletal muscle cells, poloxamer 188 (P188; an 8. Membrane damage is often manifested clinically by release of intracellular contents into the intravascular space (5), one of the clinical hallmarks of major electrical trauma. Skeletal muscle and peripheral nerve necrosis appears to be the primary cause of the high amputation rates associated with electrical trauma. We have postulated that, in the majority of victims, cell membrane permeabilization is the most important pathophysiologic event leading to tissue death (4,6,7) and, therefore, effective therapy for victims of electric shock must reestablish cell membrane structural integrity.Because membranes form spontaneously when surfactants (amphiphiles) are mixed in an aqueous solvent at sufficient concentration, we hypothesized that it may be possible to seal damaged cell membranes by exposing them to adequate concentrations of a noncytotoxic nonionic surfactant, possibly by incorporation of the surfactant into the membrane defects. In a preliminary test of this concept, we found that an 8.4-kDa nonionic synthetic surfactant, poloxamer 188 (P188), which has been clinically accepted for human intravenous administration, effectively sealed electroporated membranes of cultured skeletal muscle cells when used in concentrations >0.5 mg/ml (8, 9). We also noted that sealing the membrane enhanced cell survival as measured by vital dye [i.e., carboxyfluorescein (CF) and trypan blue] assays. The ability of P188 to bind to damaged membranes has been suggested in previous studies (10, 11).The purposes of this investigation were to determine whether the observed membrane effects of P188 on isolated cells were relatively specific to its molecular properties by comparing P188 with a neutral polysaccharide known to adsorb on the lipid bilayer (12), to determine whether the P188 and neutral polysaccharide would also reach damaged cell membranes in situ via intravenous administration and seal them after electropermeabilization, and, most important, to determine whether membrane sealing could prevent tissue necrosis following electrical injury. MATERIALS AND METHODS

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