THE EFFECT OF PERSON-ENVIRONMENT FIT ON THE PSYCHOLOGICAL WELL-BEING OF PSYCHIATRIC AIDES WORKING IN A STATE HOSPITAL (COPING RESOURCES, SOCIAL SUPPORT, OCCUPATIONAL STRESS, LOCUS-OF-CONTROL)

This study addressed two purposes: (1) to determine the effect of person-environment fit on the psychological well-being of psychiatric aides and (2) to determine what role the coping resources of social support and control have on the above relationship. Two hundred and ten psychiatric aides working in a state hospital in Texas responded to a questionnaire pertaining to these issues.^ Person-environment fit, as a measure of occupational stress, was assessed through a modified version of the Work Environment Scale (WES). The WES subscales used in this study were: involvement, autonomy, job pressure, job clarity, and physical comfort. Psychological well-being was measured with the General Well-Being Schedule which was developed by the National Center for Health Statistics. Co-worker and supervisor support were measured through the WES and finally, control was assessed through Rotter's Locus of Control Scale.^ The results of this study were as follows: (1) all person-environment (p-e) dimensions appeared to have linear relationships with psychological well-being; (2) the p-e fit - well-being relationship did not appear to be confounded by demographic factors; (3) all p-e fit dimensions were significantly related to well-being except for autonomy; (4) p-e fit was more strongly related to well-being than the environmental measure alone; (5) supervisor support and non-work related support were found to have additive effects on the relationship between p-e fit and well-being, however no interaction or buffering effects were observed; (6) locus of control was found to have additive effects in the prediction of well-being and showed interactive effects with work pressure, involvement and physical comfort; and (7) the testing of the overall study model which included many of the components mentioned above yielded an R('2) = .27.^ Implications of these findings are discussed, future research suggested and applications proposed. ^

RUNOFF FROM COAL PILES: EFFECTS ON THE ENVIRONMENT AND THE PUBLIC'S HEALTH

The use of coal for fuel in place of oil and natural gas has been increasing in the United States. Typically, users store their reserves of coal outdoors in large piles and rainfall on the coal creates runoffs which may contain materials hazardous to the environment and the public's health. To study this hazard, rainfall on model coal piles was simulated, using deionized water and four coals of varying sulfur content. The simulated surface runoffs were collected during 9 rainfall simulations spaced 15 days apart. The runoffs were analyzed for 13 standard water quality parameters, extracted with organic solvents and then analyzed with capillary column GC/MS, and the extracts were tested for mutagenicity with the Ames Salmonella microsomal assay and for clastogenicity with Chinese hamster ovary cells.^ The runoffs from the high-sulfur coals and the lignite exhibited extremes of pH (acidity), specific conductance, chemical oxygen demand, and total suspended solids; the low-sulfur coal runoffs did not exhibit these extremes. Without treatment, effluents from these high-sulfur coals and lignite would not comply with federal water quality guidelines.^ Most extracts of the simulated surface runoffs contained at least 10 organic compounds including polycyclic aromatic hydrocarbons, their methyl and ethyl homologs, olefins, paraffins, and some terpenes. The concentrations of these compounds were generally less than 50 (mu)g/l in most extracts.^ Some of the extracts were weakly mutagenic and affected both a DNA-repair proficient and deficient Salmonella strain. The addition of S9 decreased the effect significantly. Extracts of runoffs from the low-sulfur coal were not mutagenic.^ All extracts were clastogenic. Extracts of runoffs from the high-sulfur coals were both clastogenic and cytotoxic; those from the low-sulfur coal and the lignite were less clastogenic and not cytotoxic. Clastogenicity occurred with and without S9 activation. Chromosomal lesions included gaps, breaks and exchanges. These data suggest a relationship between the sulfur content of a coal, its mutagenicity and also its clastogenicity.^ The runoffs from actual coal piles should be investigated for possible genotoxic effects in view of the data presented in this study.^

THE HISTONE DEACETYLASE INHIBITOR, MS-275, SENSITIZES METASTATIC OSTEOSARCOMA TO FASL-INDUCED CELL DEATH: A ROLE FOR C-FLIP

The purpose of this study was to determine the effects of the histone deacetylase inhibitor, MS-275, on the Fas signaling pathway and susceptibility of osteosarcoma (OS) to Fas ligand (FasL)-induced cell death. OS metastasizes almost exclusively to the lungs. We have shown that Fas expression in OS cells is inversely correlated with their metastatic potential. Fas+ cells are rapidly eliminated when they enter the lungs via interaction with FasL, which is constitutively expressed in the lungs. Fas- OS cells escape this FasL-induced apoptosis and survive in the lung microenvironment. Moreover, upregulation of Fas in established OS lung metastases results in tumor regression. Therefore, agents that upregulate Fas expression or activate the Fas signaling pathway may have therapeutic potential. Treatment of Fas- metastatic OS cell lines with 2 μM MS-275 sensitized cells to FasL-induced cell death in vitro. We found that MS-275 did not alter the expression of Fas on the cell surface; rather it resulted in increased levels of Fas within the membrane lipid rafts, as demonstrated by an increase in Fas expression in detergent insoluble lipid raft fractions. We further demonstrated that following MS-275 treatment, Fas colocalized with GM1+ lipid rafts and that there was a decrease in c-FLIP (cellular FLICE-inhibitory protein) mRNA and protein. Downregulation of c-FLIP correlated with caspase activation and apoptosis induction. Transfection of cells with shRNA to c-FLIP also resulted in the localization of Fas to lipid rafts. These studies indicate that MS-275 sensitizes OS cells to FasL by upregulating the expression of Fas in membrane lipid rafts, which correlated with the downregulation of c-FLIP. Treatment of nu/nu-mice with established OS lung metastases with oral MS-275 resulted in increased apoptosis, a significant inhibition of c-FLIP expression in tumors and tumor regression. Histopathological examination of mice showed no significant organ toxicity. Overall, these results suggest that the mechanism by which MS-275 sensitizes OS cells and lung metastases to FasL-induced cell death may be by a reduction in the expression of c-FLIP.