Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder associated with vascular dysfunction and increased cardiovascular risk. This study aims to investigate the dysregulation of vascular tone in PCOS, focusing on the imbalance between vasodilators (nitric oxide [NO] and apelin) and vasoconstrictors (noradrenaline and reduced prostacyclin). By examining these factors, the study seeks to elucidate their contribution to endothelial dysfunction and cardiovascular complications in PCOS patients. Forty-four patients diagnosed with PCOS according to the 2003 Rotterdam Criteria, along with 44 healthy controls, were included in the study. Ultrasound evaluations were performed on all volunteers. Serum NO, apelin, noradrenaline, and prostacyclin levels were measured using commercial enzyme-linked immunosorbent assay (ELISA) kits. Additionally, routine biochemical, hormonal, and glycated hemoglobin analyses were conducted on all samples. There was no statistically significant difference between the PCOS and control groups in terms of marital status, age, and body mass index (BMI) (p > 0.05). Compared to the control group (83.85 ± 22.65 µmol/L, 190.88 ± 16.44 ng/L, and 24.63 ± 4.59 ng/L, respectively), NO, apelin, and noradrenaline concentrations were significantly higher in patients with PCOS (104.35 ± 44.96 µmol/L, 379.57 ± 40.11 ng/L, and 27.48 ± 5.36 ng/L, respectively) (p < 0.01). In contrast, prostacyclin concentrations were significantly lower in patients with PCOS (5.85 ± 1.28 ng/L) compared to the control group (6.78 ± 1.99 ng/L) (p = 0.011). Additionally, a statistically significant difference was found between the PCOS and control groups in FSH, LH, testosterone, SHBG, glucose, and HDL levels (p < 0.05). The disrupted balance between vasodilation and vasoconstriction in PCOS, driven by altered levels of NO, apelin, noradrenaline, and prostacyclin, contributes to endothelial dysfunction and increased cardiovascular risk. These molecular disturbances underline the need for targeted therapeutic strategies aimed at restoring vascular homeostasis in PCOS patients.

Background and Objectives: Heat shock proteins (HSPs) are stress proteins. The endogenous nitric oxide (NO) synthase inhibitor asymmetric dimethyl arginine (ADMA) is a mediator of endothelial dysfunction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus causes endothelial dysfunction and coagulopathy through severe inflammation and oxidative stress. Using these markers, we analyzed the prognostic value of serum ADMA and HSP-90 levels for early prediction of severe coronavirus disease (COVID-19) patients. Materials and Methods: A total of 76 COVID-19 patients and 35 healthy control subjects were included in this case–control study. COVID-19 patients were divided into two groups: mild and severe. Results: Serum ADMA and HSP-90 levels were significantly higher in the COVID-19 patients compared to the control subjects (p < 0.001). Additionally, serum ADMA and HSP-90 levels were determined to be higher in a statistically significant way in severe COVID-19 compared to mild COVID-19 (p < 0.001). Univariable logistic regression analysis revealed that ADMA and HSP-90, respectively, were independent predictors of severe disease in COVID-19 patients (ADMA (OR = 1.099, 95% CI = 1.048–1.152, p < 0.001) and HSP-90 (OR = 5.296, 95% CI = 1.719–16.316, p = 0.004)). When the cut-off value for ADMA was determined as 208.94 for the prediction of the severity of COVID-19 patients, the sensitivity was 72.9% and the specificity was 100% (AUC = 0.938, 95%CI = 0.858–0.981, p < 0.001). When the cut-off value for HSP-90 was determined as 12.68 for the prediction of the severity of COVID-19 patients, the sensitivity was 88.1% and the specificity was 100% (AUC = 0.975, 95% CI= 0.910–0.997, p < 0.001). Conclusions: Increased levels of Heat shock proteins-90 (HSP-90) and ADMA were positively correlated with increased endothelial damage in COVID-19 patients, suggesting that treatments focused on preventing and improving endothelial dysfunction could significantly improve the outcomes and reduce the mortality rate of COVID-19. ADMA and HSP-90 might be simple, useful, and prognostic biomarkers that can be utilized to predict patients who are at high risk of severe disease due to COVID-19.

Background and Objectives: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by acute exacerbations. Systemic inflammation and oxidative stress play an important role in the pathogenesis of COPD. Exacerbations in COPD reduce the quality of life and are associated with rapid disease progression. Galectin-3 is a beta-galactoside-binding lectin of approximately 30 kDa with pro-inflammatory and pro-fibrotic properties. This study aims to analyze the efficacy of serum galectin-3 in predicting exacerbations in COPD patients. Materials and Methods: Baseline demographic and clinical characteristics of all patients were recorded and blood samples were collected. A total of 58 consecutive COPD patients, including 28 patients (19 male and 9 female) with stable COPD and 30 patients (23 male and 7 female) with acute exacerbation of COPD (AECOPD), were included in the study. Results: Serum galectin-3 levels were significantly higher in the AECOPD group compared to the stable COPD group. A logistic regression analysis revealed that increased galectin-3 levels and disease duration were independent predictors of COPD exacerbation (OR = 5.322, 95% CI: 1.178–24.052, p = 0.03; and OR = 1.297, 95% CI: 1.028–1.635, p = 0.028; respectively). Conclusions: The results of our study demonstrated that Galectin-3 was a strong and independent predictor of exacerbations in COPD patients.

Fibromyalgia syndrome (FMS) is a chronic pain disorder characterized by widespread musculoskeletal pain, fatigue, and cognitive dysfunction. Although its exact pathophysiology remains unclear, emerging evidence suggests that endoplasmic reticulum (ER) stress and oxidative stress play significant roles in its development. This study aimed to investigate the involvement of ER stress in FMS by evaluating key ER stress markers and oxidative stress parameters in patients with FMS. A total of forty-four FMS patients and matched healthy controls were included in the study. Serum levels of ER stress markers were measured using enzyme-linked immunosorbent assay (ELISA). Additionally, oxidative stress markers were assessed to examine their relationship with ER stress in FMS. The ER stress parameters were significantly higher in the FMS group compared to controls. Furthermore, oxidative stress markers were elevated, reinforcing the interconnection between ER stress and oxidative stress in FMS pathogenesis. These findings suggest that ER stress plays a crucial role in the pathophysiology of FMS, likely contributing to disease progression through oxidative stress-related mechanisms. Targeting ER stress and oxidative stress pathways may represent a promising therapeutic strategy for FMS management. Future studies should focus on large-scale clinical investigations to further elucidate these pathways and develop effective treatment approaches.