Background and Objectives: Migraine is the most common primary headache disorder worldwide, negatively affecting quality of life and limiting the functionality of individuals. Although its pathogenesis is not fully understood, it is known that activation of the trigeminovascular system, neurogenic inflammation, and oxidative stress are among the main components of migraine. In this context, we aimed to investigate the possible role of the nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway, which plays a key role in the regulation of cellular oxidative stress, in the development of chronic diseases such as migraine. Materials and Methods: In this study, the oxidative stress parameters total oxidant level (TOS), total antioxidant level (TAS), and oxidative stress index (OSI) and changes in the Nrf2/Keap1 signaling pathway were analyzed in migraine patients. Results: The results showed that Keap1 levels were significantly higher in migraine patients compared with the control group, whereas the Nrf2 and TAS levels were low. In addition, increased levels of oxidized LDL (oxLDL) and glycogen synthase kinase-3 beta (GSK3B), which are oxidative stress markers, confirmed that the oxidative stress burden was high in migraine patients. The fact that OSI values were significantly higher in migraine patients clearly demonstrates that systemic oxidative stress was out of balance in these individuals. Conclusions: In conclusion, this study reveals that oxidative stress and the Nrf2/Keap1 signaling pathway play an important role in the pathogenesis of migraine. Decreased Nrf2 activity and increased Keap1 levels suggest that the antioxidant defense system is insufficient in migraine patients. These findings suggest that the Nrf2/Keap1 signaling pathway may be considered as a potential target for migraine treatment and that the development of new treatment strategies to reduce oxidative stress may be beneficial.

Background/Objectives: Various pathophysiological mechanisms play a role in the development of cardiovascular diseases (CVDs). There is a need for new biomarkers that can complement existing clinical findings, particularly in the early diagnosis and prognostic assessment of coronary artery disease (CAD) and that can also contribute to more effective management of the diagnosis and treatment process. Therefore, both blood and pericardial fluid samples can provide important diagnostic information. This study aims to investigate Stromal Cell-Derived Factor 4 (SDF4) levels and thiol/disulfide homeostasis in the blood and pericardial fluid of patients with established CAD undergoing open-heart surgery with cardiopulmonary bypass (CPB), in order to better characterize oxidative stress-related and redox-mediated pathophysiological processes associated with the development and progression of coronary heart disease. Comparisons with a healthy control group were performed to elucidate disease-related biochemical alterations rather than to propose these markers as diagnostic tools for CAD. Methods: In this study, intraoperatively collected venous blood and pericardial fluid samples from 45 patients undergoing on-pump coronary artery bypass grafting were analyzed. SDF4 levels were measured using enzyme-linked immunosorbent assay (ELISA), while thiol–disulfide homeostasis was assessed via spectrophotometric analysis. Results: The study revealed statistically significant differences in parameters such as SDF-4, native thiol, total thiol, disulfide, and disulfide/total thiol ratio among the control, patient serum, and pericardial fluid groups (p < 0.05). Notably, SDF-4 and disulfide levels were elevated, while thiol levels were reduced in the pericardial fluid group, suggesting increased oxidative stress and disrupted redox balance. Principal Component Analysis (PCA) and Variable Importance in Projection (VIP) analyses successfully demonstrated the discriminative power of these parameters among the groups. Conclusions: The increased SDF-4 levels and disturbances in the thiol–disulfide balance observed in this study indicate elevated oxidative stress and impaired cellular redox homeostasis in CAD. These findings suggest that SDF-4 and thiol–disulfide parameters may serve as important biochemical markers in the pathophysiology of CVD and hold potential as diagnostic and prognostic biomarkers.

Background: It has been shown that drugs used parenterally cause errors in immunosuppressant concentrations measured by LC-MS / MS method. It is yet unknown whether this measurement error is due to drug-drug interaction or analytical interference. Objective: The aim of this study is to investigate the possible interaction and inhibition concentrations of broad-spectrum antibiotics (ertapenem, meropenem, imipenem) with 4 different immunosuppressants (tacrolimus, sirolimus, everolimus, cyclosporine A) by molecular docking. Method: The docking results of ertapenem, meropenem, and imipenem-cilastatin drugs, which are frequently used in intensive care units and wards, were analyzed with the Autodock 4.2 program. Binding energy levels and inhibition concentrations were recorded. Results: The highest binding energies of the most stable conformations, providing the best compatibility among the active ingredients, belong to cilastatin. The interaction energy of cilastatin with sirolimus in 320 conformations was calculated as -4.08 kcal/mol. Sirolimus interacted with ertapenem at -3.43, imipenem at -2.53, and meropenem at -3.84 kcal/mol. According to these values, the receptor, which is the most compatible host with all ligand molecules, is sirolimus. The least interaction energy value was calculated between cyclosporine and imipenem (-1.12 kcal / mol). Conclusion: Concerning the most stable conformations of models docked with Autodock tools, it has been determined that carbapenems interact with immunosuppressants. Since the detected inhibition concentration levels can be seen in blood samples taken immediately after carbapenem injection, immunosuppressant measurement is recommended before the use of carbapenem in immunosuppressant monitoring of transplant patients.