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Background The intricate interplay between work-related stress and its physiological impact has drawn extensive research attention. Dehydroepiandrosterone sulphate (DHEA-S) emerges as a potential biomarker reflecting stress-related endocrine changes. Aims This cross-sectional study aimed to examine the association between job demands and DHEA-S levels among healthcare workers. The study also explored potential correlations between DHEA-S levels and psychophysical symptoms commonly linked to work-related stress. Methods A sample of 488 healthcare workers from a local health authority participated. Job demands were measured using the Demands scale of the Health and Safety Management Standards Indicator Tool. DHEA-S levels and symptom prevalence were assessed through serum analysis and questionnaires, respectively. Results Workers exposed to high job demands exhibited significantly lower DHEA-S levels compared to those with low job demands. Psychophysical symptoms, including sleep disorders, depression, and headache, were more prevalent in the high-demands group. DHEA-S levels showed significant negative correlations with the prevalence of all considered symptoms. Conclusions The study shows the inverse relationship between job demands and DHEA-S levels among healthcare workers, indicating that high job demands correlate with reduced DHEA-S secretion and increased symptom prevalence. The findings suggest DHEA-S as a potential biomarker for assessing the physiological consequences of work-related stress. Proactive interventions in managing job demands are crucial for promoting employee well-being and productivity in demanding work environments. By recognizing DHEA-S as a stress biomarker, organizations can effectively address stress-related health risks and implement targeted interventions for enhancing employees' overall health and work performance. [ABSTRACT FROM AUTHOR]

Increasing evidence indicates that metabolism is implicated in the control of stem cell identity. Here, we demonstrate that embryonic stem cell (ESC) behaviour relies on a feedback loop that involves the non-essential amino acid L-Proline (L-Pro) in the modulation of the Gcn2-Eif2α-Atf4 amino acid starvation response (AAR) pathway that in turn regulates L-Pro biosynthesis. This regulatory loop generates a highly specific intrinsic shortage of L-Pro that restricts proliferation of tightly packed domed-like ESC colonies and safeguards ESC identity. Indeed, alleviation of this nutrient stress condition by exogenously provided L-Pro induces proliferation and modifies the ESC phenotypic and molecular identity towards that of mesenchymal-like, invasive pluripotent stem cells. Either pharmacological inhibition of the prolyl-tRNA synthetase by halofuginone or forced expression of Atf4 antagonises the effects of exogenous L-Pro. Our data provide unprecedented evidence that L-Pro metabolism and the nutrient stress response are functionally integrated to maintain ESC identity. [ABSTRACT FROM AUTHOR]

A correction to the article "Cell Death and Differentiation," that was published in the April 10, 2015 issue is presented.