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    Excessive Weight Gain During Pregnancy Increased Ponoxarase 1 Level in Neonatal Cord Blood
    (Mdpi, 2025) Ege, Serhat; Akduman, Hasan; Asir, Aysegul; Korak, Tugcan
    Maternal obesity is increasingly recognized as a risk factor for adverse fetal outcomes, primarily through its association with heightened oxidative stress. This study aimed to evaluate oxidative stress markers in umbilical cord blood of neonates born to obese mothers. Sixty-three pregnant women, who were of normal weight at the start of pregnancy but classified as obese at term, were included. Umbilical cord blood samples were collected immediately post-delivery and analyzed for serum oxidative stress markers (total oxidant status (TOS), total antioxidant status (TAS), paraoxanase (PON), aryl esterase, thiol, and catalase activities). Protein interaction networks were generated using Cytoscape (v3.10.3), and the overlapping proteins were further analyzed for functional annotations with ShinyGO (0.80). The top ten significantly enriched pathways were identified with a false discovery rate (FDR) threshold of <0.05. Significant associations were found between maternal BMI change and paraoxonase 1 (PON1) levels in umbilical cord blood, while no correlation was observed with other oxidative (total oxidant status) and antioxidant markers (total antioxidant status, aryl esterase, thiol, and catalase). Additionally, the correlation analysis showed a significant relationship between BMI change and fetal gestational age, but not with other demographic or clinical features. A total of 24 common protein interactors associated with PON1, obesity, and oxidative stress were identified. Functional annotation analysis revealed significant enrichment in antioxidant and oxidoreductase activities, along with pathways involved in insulin resistance, AGE-RAGE signaling, and atherosclerosis. Maternal obesity may specifically affect PON1 activity, potentially serving as a compensatory response to oxidative stress in neonates, suggesting PON1 as a possible biomarker for oxidative stress-related metabolic disturbances in neonates of obese mothers, with implications for monitoring and managing pregnancy outcomes in obese populations.
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    Gallic acid showed neuroprotection against endoplasmic reticulum stress in rats
    (Acta Cirurgica Brasileira, 2025) Karaaslanli, Abdulmutalip; Tuncer, Mehmet Cudi; Asir, Firat; Korak, Tugcan
    Purpose: We aimed to investigate the role of gallic acid treatment on spinal cord tissues after spinal cord injury (SCI) and its relationship with endoplasmic reticulum (ER) stress by histochemical, immunohistochemical, and in-silico techniques. Methods: Thirty female Wistar albino rats were divided into three groups: sham, SCI, and SCI+gallic acid. SCI was induced by dropping a 15-g weight onto the exposed T10-T11 spinal cord segment. The SCI+gallic acid group received 25 mg/kg of gallic acid intraperitoneally daily for one week. Histopathological, immunohistochemical, and silico analyses were performed. Results: Histological analysis revealed improved neural cell survival and tissue integrity in the SCI+gallic acid group compared to the SCI group. Caspase-12 expression was significantly increased in the SCI group, indicating elevated ER stress and apoptosis. Gallic acid treatment resulted in a marked reduction in caspase-12 expression in neurons, neuroglia, and endothelial cells, suggesting decreased ER stress. Conclusion: Gallic acid exhibits significant neuroprotective effects against ER stress and cellular damage in a rat model of SCI. The in-silico analysis revealed apoptotic and immune-related pathways in which gallic acid showed neuroprotective effects by regulating caspase-12. These results suggest that gallic acid may be a promising therapeutic agent for mitigating secondary damage post-SCI.
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    The Immunohistochemical and Bioinformatics Analysis of the Placental Expressions of Vascular Cell Adhesion Protein 1 (VCAM-1) and High Mobility Group Box 1 (HMGB1) Proteins in Gestational Diabetic Mothers
    (Georg Thieme Verlag Kg, 2024) Oglak, Suleyman Cemil; Asir, Firat; Yilmaz, Emine Zeynep; Bolluk, Gokhan; Korak, Tugcan; Agacayak, Elif
    Objective We aimed to examine both the expression levels of high mobility group box 1 (HMGB1) and vascular cell adhesion molecule-1 (VCAM-1) proteins in the placentas of pregnant women with gestational diabetes mellitus (GDM) and control groups by immunohistochemical (IHC) method. Material and methods An experimental case-control study was conducted, including 40 pregnant women complicated with GDM and 40 healthy pregnant women. Placental tissues obtained following cesarean delivery were subjected to routine tissue monitoring. The placental sections were stained with VCAM-1 and HMGB1 immunostains and subjected to IHC examination under a light microscope. H-score (HS) was used to evaluate the results of IHC staining by semi-quantitative analysis. Pathway analysis in Cytoscape software identified GDM-associated proteins within HMGB1 and VCAM-1 interaction networks, followed by GO analysis to explore associated biological processes. Results Placental HGMB1 expression was significantly increased in the GDM group compared to the control group (p<0.001). However, placental VCAM-1 expression was found to be statistically similar in GDM and control groups (p=0.584). The shared 19 proteins were identified between HMGB1 and GDM, and 13 between VCAM-1 and GDM, with notable GO biological process terms such as immune system activation for HMGB1 and interleukin-6 regulation for VCAM-1 associated with GDM. Conclusion We consider that GDM-related inflammation and oxidative stress may contribute to tissue damage and inflammation by increasing placental HMGB1 expression. The blockade of HMGB1 and its receptors might represent a promising therapeutic approach to control inflammation in GDM. Understanding the distinct roles of HMGB1 and VCAM-1 may provide valuable insights for the development of targeted therapies aimed at mitigating the inflammatory processes associated with GDM and improving maternal and fetal outcomes.
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    Investigation of Vitamin D Levels in Men with Suspected Infertility
    (Mdpi, 2024) Asir, Firat; Duran, Senem cetin; Afsin, Muhammet; Duran, Enis; Korak, Tugcan; Sahin, Firat
    Male infertility may be caused by an impaired sperm functionality, with insufficient vitamin D levels affecting the quantity and development of motile sperm. Given the influence of vitamin D on vital aspects of male infertility, this study aimed to investigate the correlation between vitamin D levels and male infertility, along with exploring the possible mechanism of action. A total of 306 male participants were included. Semen samples were collected and analyzed for semen parameters with demographic features. Patients were classified into two groups based on vitamin D levels of <20 ng/mL (low) and >= 20 ng/mL (high). The Super-PRED, Swiss TargetPrediction, GeneCards, and DisGeNET databases were utilized to retrieve potential molecular targets associated with both vitamin D and male infertility, while the STRING database was employed for constructing protein-protein interaction (PPI) networks and conducting a functional enrichment analysis. A total of 146 patients (47.71%) showed low vitamin D levels and 160 patients (52.29%) had high vitamin D levels. Vitamin D was not strongly influenced by demographic parameters. Vitamin D demonstrated significant positive correlations with type A and B sperm motility. Conversely, it exhibited significant negative correlations with type C and D sperm motility. Hormones (thyroid-stimulating hormone, follicle-stimulating hormone, prolactin, luteinizing hormone, estradiol) were not significantly associated with vitamin D; however, testosterone was significantly positive correlated with vitamin D. Notably, no significant correlation was found between vitamin D levels and iron, ferritin, hemoglobin, hematocrit, calcium, magnesium, and phosphorus levels. The functional annotations of potential vitamin D targets associated with male infertility primarily indicated involvement in regulating infection, the immune response, forkhead box O (FOXO) and hypoxia-inducible factor 1 (HIF1) signals in male infertility. Adequate vitamin D levels are associated with an improved reproductive health, evidenced by positive correlations with hormone levels and sperm motility. Specifically, the FOXO and HIF-1 signaling pathways may be effective in the potential molecular mechanisms underlying the impact of vitamin D on male infertility and/or in the significant correlations identified.
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    Placental Vimentin Expression in Preeclampsia and Gestational Diabetes Mellitus
    (2024) Asır, Fırat; Oglak, Suleyman Cemil; Korak, Tugcan; Tas, Fatih; Yılmaz, Mehmet; Erdemcı, Fikri; Sahın, Firat
    OBJECTIVE: This study investigated vimentin expression in placentas of patients with preeclampsia and gestational diabetes mellitus (GDM). STUDY DESIGN: Placentas of preeclamptic women (n=25), women with GDM (n=25), and control cases (n=25) were enrolled in this study. Placental samples were fixed in zinc-formalin and further processed for paraffin wax tissue embedding. Demographic and laboratory parameters of patients were recorded. Vimentin immune activity was analyzed in the placental sections with immunohistochemistry. Sections were imaged and analyzed under a light microscope. A semiquantitative measurement was done be- tween groups by comparing the Vimentin signal and significance was calculated. Network construction and pathway enrichment analysis were conducted using Cytoscape (v3.10.1) and ShinyGO, respectively. RESULTS: Vimentin expression was high in the placental sections of the control group. The preeclamp- sia group showed positive Vimentin expression in cytotrophoblast and syncytiotrophoblast cells and con- nective tissue of placental villi in the preeclampsia group. Vimentin expression was generally recorded as negative in placental villi, fibrinoid substances, and connective tissue cells in the GDM group. Bioinformatic analysis showed that the AGE-RAGE signaling pathway and cancer-related pathways were mainly observed in Vimentin-associated pathways, which finally activate inflammatory pathways in both preeclampsia and GDM. CONCLUSION: Vimentin expression patterns in placental tissue sections reveal nuanced regulatory mechanisms, emphasizing the need for further exploration into the functional roles of vimentin in pla- cental physiology and pathology.