The circadian rhythm of cortisol, a key hormone essential for maintaining metabolic balance and stress homeostasis, is profoundly disrupted by night-shift work. This narrative review examines the physiological mechanisms underlying cortisol regulation, the effects of shift work on its circadian rhythm, the associated health risks, and potential mitigation strategies. Night-shift work alters the natural secretion pattern of cortisol, leading to dysregulation of the hypothalamic–pituitary–adrenal axis, which in turn can contribute to metabolic disorders, cardiovascular diseases, and impaired cognitive function. Understanding the physiological pathways mediating these changes is crucial for developing targeted interventions to mitigate the adverse effects of circadian misalignment. Potential strategies, such as controlled light exposure, strategic napping, and personalized scheduling, may help to stabilize cortisol rhythms and improve health outcomes. This review aims to provide insights that can guide future research and inform occupational health policies for night-shift workers by addressing these challenges.

Both fibroblast growth factor 9 (Fgf9) and Kit Ligand (Kl) signal through tyrosine kinase receptors, yet they exert opposite effects on meiotic differentiation in postnatal spermatogonia, Fgf9 acting as a meiosis-inhibiting substance and Kl acting as a promoter of the differentiation process. To understand the molecular mechanisms that might underlie this difference, we tried to dissect the intracellular signaling elicited by these two growth factors. We found that both Fgf9 and Kl stimulate Erk1/2 activation in Kit+ (differentiating) spermatogonia, even though with different time courses, whereas Kl, but not Fgf9, elicits activation of the Pi3k-Akt pathway. Sustained Erk1/2 activity promoted by Fgf9 is required for induction of the autocrine Cripto-Nodal-Smad2/3 signaling loop in these cells. Nodal signaling, in turn, is essential to mediate Fgf9 suppression of the meiotic program, including inhibition of Stra8 and Scp3 expression and induction of the meiotic gatekeeper Nanos2. On the contrary, sustained activation of the Pi3k-Akt pathway is required for the induction of Stra8 expression elicited by Kl and retinoic acid. Moreover, we found that Kl treatment impairs Nodal mRNA expression and Fgf9-mediated Nanos2 induction, reinforcing the antagonistic effect of these two growth factors on the meiotic fate of male germ cells.

Thyroid nodules are a common clinical finding, with their prevalence influenced by multiple environmental and occupational factors, including exposure to ionizing radiation. Healthcare workers, particularly those operating in radiology, nuclear medicine, interventional cardiology, and radiation oncology, are potentially at increased risk due to chronic low-dose radiation exposure. This review aims to evaluate the current evidence regarding the association between occupational radiation exposure and the development of thyroid nodules among healthcare professionals. The findings suggest a higher prevalence of thyroid nodules in radiation-exposed workers compared to the general population, although data heterogeneity and methodological limitations exist. Factors such as the duration of exposure, radiation protection practices, and frequency of monitoring play critical roles in modulating the individual risk. While some studies report no significant difference in malignancy rates, the increased detection of nodules underlines the need for regular thyroid surveillance in at-risk populations. Further longitudinal and multicentric studies are warranted to clarify the causality and guide preventive strategies. This review highlights the importance of occupational health protocols, including radiation shielding and periodic thyroid evaluation, in safeguarding the long-term endocrine health of healthcare workers.

Serum and glucocorticoid-inducible kinase 1 (SGK1) is a ubiquitous kinase with cytoprotective and immune-specific functions. Parkinson's disease (PD) animal models disclosed interactions between SGK1 and the critical pathogenic pathways of the disease, whereas human-based evidence is lacking. We investigated the SGK1 contribution to the biological dynamics of PD ex vivo, at immune and systemic level. Thirty-two well-phenotyped PD patients and 34 controls were enrolled. Peripheral blood mononuclear cells (PBMCs) and serum were obtained. PBMCs levels of SGK1, α-synuclein total and oligomeric forms (α-syn^tot, α-syn^olig) were measured by Western blot and ELISA, respectively. SGK1 levels were tested in the serum by ELISA. Group differences were assessed using age-adjusted, rank-based linear regression models; ROC analysis was performed using age-adjusted PBMC SGK1 residuals and a Youden-derived cutpoint; associations with clinical variables were tested using age-adjusted regressions. PD PBMCs exhibited lower SGK1 (p < 0.001) and higher α-syn^olig levels than controls (p = 0.026). SGK1 serum levels were also lower in PD patients (p = 0.040). ROC analysis showed that PBMC SGK1 significantly discriminated PD from controls (AUC = 0.85,[95 % CI 0.75-0.95],p < 0.001). The optimal cutpoint yielded a sensitivity of 1.00 and a specificity of 0.60. No significant correlations were found between biological and clinical parameters. In PD patients, SGK1 was downregulated in both PBMCs and serum. Given the preliminary nature of these findings and the co-occurrence of α-syn^olig accumulation in leukocytes, common mechanistic pathways might be supposed, although pending confirmation. Nevertheless, SGK1 emerged as a potential target in PD, for both biomarker and therapeutic purposes.

Background: Fasting plasma glucose, glycated hemoglobin (HbA1c), and oral glucose tolerance testing remain central to the diagnosis and monitoring of dysglycemia, but they mainly reflect the average glycemic exposure or discrete time-point measurements and may not capture intraday and interday glucose fluctuations. Glycemic variability (GV) has been associated with oxidative stress, endothelial dysfunction, inflammation, and diabetes-related complications, although much of the evidence derives from experimental, clinical, and diabetes-care settings rather than occupational cohorts. Aim: This narrative review examines the physiological basis, measurement, and potential occupational relevance of GV and continuous glucose monitoring (CGM) in working populations. Methods: Literature was narratively selected from biomedical databases, major guidelines, consensus statements, and occupational-health sources, prioritizing reviews, clinical guidelines, cohort studies, mechanistic studies, and CGM studies. No systematic search, risk-of-bias assessment, or quantitative synthesis was performed. Main findings: CGM is an established technology in selected diabetes-care contexts and provides metrics such as coefficient of variation, time in range, time above range, and time below range. Its use in occupational medicine, however, remains investigational outside selected clinical circumstances. Work-related factors such as shift work, circadian disruption, sleep loss, psychosocial stress, irregular meal timing, sedentary behavior, and variable physical workload may influence glucose regulation, but direct evidence linking these exposures to CGM-measured GV in workers remains limited. Implications: Potential applications include research on occupational determinants of metabolic health, monitoring of workplace lifestyle interventions, and individualized management of workers with diabetes in safety-sensitive roles, provided that consent, confidentiality, clinical follow-up, equity, and data-governance safeguards are ensured. Conclusions: GV assessment may complement traditional metabolic markers in selected occupational-health contexts, but routine CGM-based surveillance of general worker populations is not currently supported by sufficient evidence. Further longitudinal and interventional studies are required.