Attention and automation: New perspectives on mental underload and performance

There is considerable evidence in the ergonomics literature that automation can significantly reduce operator mental workload. Furthermore, reducing mental workload is not necessarily a good thing, particularly in cases where the level is already manageable. This raises the issue of mental underload, which can be at least as detrimental to performance as overload. However, although it is widely recognized that mental underload is detrimental to performance, there are very few attempts to explain why this may be the case. It is argued in this paper that, until the need for a human operator is completely eliminated, automation has psychological implications relevant in both theoretical and applied domains. The present paper reviews theories of attention, as well as the literature on mental workload and automation, to synthesize a new explanation for the effects of mental underload on performance. Malleable attentional resources theory proposes that attentional capacity shrinks to accommodate reductions in mental workload, and that this shrinkage is responsible for the underload effect. The theory is discussed with respect to the applied implications for ergonomics research

A vldl response element in the promoter region of the human pai-1 gene implicated in the impaired fibrinolysis of hypertriglyceridaemia

Increased plasma plasminogen activator inhibitor-1 (PAI-1) activity is a common finding in patients with coronary heart disease (CHD), particularly in young post-infarction patients with hypertriglyceridaemia, and is associated with recurrence of cardiovascular events. Both environmental and genetic factors contribute to determine plasma PAI-1 activity. A striking feature of PAI-1 is its positive association with the very low density lipoprotein (VLDL) triglycéride concentration. In the present study, we support the notion that a common 4G/5G polymorphic region in the PAI-1 promoter is involved in an allele-specific response to triglycérides. The slope of the regression line was steeper among individuals who were homozygous for the 4G allele as compared to individuals who were homozygous for the 5G allele. Transfection and DMA binding studies showed that the two proteins that previously been shown to bind to the 4G and 5G sequences (Eriksson et al. (1995) Proc. Natl. Acad. Sei. USA 92, 1851-1855), are not directly involved in an activation of the PAI-1 promoter mediated by VLDL. However, by transfection assay, VLDL was shown to induce transcription of the PAI-1 promoter in HUVEC:s. Maximum induction was obtained at 0.075 mg VLDL/ml culture medium. A promoter construct containing the 4G allele showed a slightly higher promoter activity in response to VLDL (3.8 fold induction) than did the promoter containing the 5G allele (2.3 fold induction). To localize the VLDL-response element, transfection studies with promoter deletions together with mobility shift assay and footprinting studies were performed. VLDL-induction of PAI-1 in endothelial cells was found to be caused by transcriptional activation mediated by a response element in the PAI-1 promoter located downstream and adjacent to the 4G/5G polymorphic site. Competitive binding of the factors binding to the polymorphic 4G/5G site and the VLDL induced factor could explain the allele specific response