ACTA ENDOCRINOLOGICA (BUC)

Background. Hyperglycaemia during acute ischaemic stroke (AIS) has been associated with poorer outcomes yet attempts to normalise glucose have not demonstrated clinical benefit. One proposed explanation is that the participants are not routinely stratified by the pre-stroke glycaemic status (diabetic hyperglycaemia [DHG], non-diabetic hyperglycaemia [NDHG]), which may contribute to heterogeneity in metabolic responses and dilute treatment effects. We compared early endocrine and inflammatory responses (insulin, C-peptide, cortisol, and cytokines) between DHG and NDHG and examined exploratory associations with stroke severity and 90-day functional outcomes. Methods. In this prospective multicentre cohort, 80 patients with AIS and hyperglycaemia (DHG or NDHG) were enrolled within 72 hours of admission. Biomarkers were measured on admission. Group comparisons were performed by diabetes status and stroke severity. Exploratory associations with 90-day functional outcome were assessed with LASSO regression. Results. Compared with DHG, NDHG was associated with higher insulin (142 vs 75 pmol/L;p<0.05), C-peptide (1.15 vs 0.87 nmol/L;p<0.05), IL-8 (23 vs 13 pg/ mL;p<0.01), and IL-6 (8 vs 3 pg/mL;p=0.094). Cortisol was numerically higher in DHG than NDHG (352 vs 271 nmol/ L;p=0.32). Within NDHG, endocrine and inflammatory measures varied by stroke severity, while remaining generally higher than DHG. Conclusion. Diabetes status was associated with differences in early endocrine and inflammatory profiles during AIS-associated hyperglycaemia. Given the observational design, single-time-point sampling, and modest sample size, these findings should be interpreted as hypothesis-generating. Future adequately powered studies with standardised sampling and detailed diabetes phenotyping are needed to determine whether diabetesstratified approaches to hyperglycaemia management and prognostic modelling improve clinical utility.

Melanoma has a significant mortality and its growing incidence is associated with important social and health care costs. Thus, investigation of the complex mechanisms contributing to emergence and development of melanoma are of real interest both in scientific research and clinical practice. Estrogens play an important role in the emergence and development of certain types of cancer, such as breast cancer, endometrial cancer and ovarian cancer, but their role in development of cutaneous melanoma is still a matter of debate. Various data suggest that increased levels of endogenous estrogens during pregnancy or exposure to exogenous estrogens by use of oral contraceptives (OCs) and hormone replacement therapy (HRT) may have a potential role in melanoma development and progression. Moreover, there were revealed several intracellular pathways which can support the connection between estrogens, estrogen receptors (ER) and melanoma. While ER-β plays an antiproliferative role, ER-α promotes cell growth and cellular atypia. Thus, inhibition of ER-β activity in the skin can increase the risk for development of cutaneous melanoma and spread of metastatic cells. However, despite recent advances in this area, the exact role and clinical implications of estrogens and estrogen receptors in melanoma are still not entirely understood and require further investigations

Diabetes is one of the most prevalent chronic disorders, associating numerous somatic and behavioral modifications. Oxytocin has been widely studied for its involvement in social behavior and psychiatric disorders. This pilot study presents a series of 3 patients with type 1 diabetes and diabetic neuropathy in which the values of plasma oxytocin, neurotensin, β-endorphins, α-MSH, substance P and orexin A were measured in comparison to 3 healthy controls with matching ages. In the diabetic patients group, there was a strong negative correlation between the value of plasma glucose and oxytocin (r=-0.99, p=0.04), respectively neurotensin (r=- 0.99, p=0.03). These values did not correlate in the control group. The results suggest that oxytocin, in conjunction with neurotensin, could be investigated as a potential early detection marker of diabetic neuropathy and, to our knowledge, this is the first report focusing on plasma oxytocin levels in patients with diabetic neuropathy.

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Context. Melanoma is the most aggressive skin cancer, with significant morbidity and mortality, and one factor that may influence the course of disease is stress. Objective. Our aim was to evaluate the effect of corticosterone, norepinephrine, epinephrine on murine B16F10 melanoma cells in vitro proliferation. Methods. B16F10 melanoma cells were treated with different concentrations of tested hormones. The proliferative capacity of melanoma cells was quantified by MTS assay and the cell viability was quantified as membrane integrity evaluation measured by lactate dehydrogenase (LDH) release. Results. B16F10 cells treated with corticosterone showed no significant changes. In contrast, norepinephrine exposure stimulated the cell proliferation (P = 0.0003). Treatment with 1 μM norepinephrine induced the highest increase in cell proliferation (OD 492 = 0.27 ± 0.02) statistically significant to both control (OD 492 = 0.17 ± 0.01; p = 0.0003), 10 nM norepinephrine (OD 492 = 0.16 ± 0.00; p = 0.0004) and 100 nM norepinephrine (OD 492 = 0.19 ± 0.01; p = 0.002). Likewise, treatment with epinephrine increased cell proliferation (p = 0.0004). Exposure to 5 μm epinephrine induced a stimulation of cell proliferation (OD 492 = 0.28 ± 0.02) significantly higher compared to controls (OD 492 = 0.17 ± 0.01; p = 0.0004), 50 nM epinephrine (OD 492 = 0.17 ± 0.00; p = 0.001) and 500 nM epinephrine (OD 492 = 0.173 ± 0.00; p = 0.001). Conclusions. Our results may open new perspectives concerning the link between stress hormones and melanoma, emphasizing a direct stimulating in vitro effect induced by catecholamines on melanoma B16F10 cells proliferation.