Browsing by Author "Korak, Tugcan"

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Placental Vimentin Expression in Preeclampsia and Gestational Diabetes Mellitus
(2024) Yılmaz, Mehmet; Oglak, Suleyman Cemil; Korak, Tugcan; Tas, Fatih; Yılmaz, Mehmet; Erdemcı, Fikri; Bolluk, Gokhan
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.
Zonisamide Ameliorated the Apoptosis and Inflammation in Cerebellar Tissue of Induced Alcohol Addiction Animal Model
(Mdpi, 2024) Asir, Firat; Erdemci, Fikri; Cankiri, Zuhal; Korak, Tugcan; Basaran, Sureyya Ozdemir; Kaplan, Ozge; Tunik, Selcuk
This study investigated the effects of zonisamide treatment on cerebellar tissues in an experimental alcohol addiction (AA) model and its potential mechanisms of action, particularly regarding apoptotic protease activating factor-1 (APAF-1) and tumor necrosis factor-alpha (TNF-alpha) expression. Thirty rats were divided into three groups: sham, ethanol (EtOH), and EtOH + zonisamide. AA was induced by administering 6 cc of EtOH orally every 8 h for 4 days. Zonisamide (100 mg/kg) was given to rats once daily before EtOH administration. Motor defects were evaluated using an open field maze. Serum TNF-alpha levels were measured from blood samples. Cerebellar sections were processed for histological examination and immunostained for APAF-1 and TNF-alpha. Protein interaction networks were constructed using Cytoscape, and functional annotations were performed with ShinyGO (version 0.80) software. The traveled area in the EtOH group was significantly reduced compared to the sham group (p = 0.0005). Rats in the EtOH + zonisamide group covered a larger area, with zonisamide treatment significantly improving locomotor ability compared to the EtOH group (p = 0.0463). Serum TNF-alpha levels were significantly elevated in the EtOH group compared to the sham group (p < 0.0001) and were significantly decreased in the EtOH + zonisamide group compared to the EtOH group (p = 0.0309). Regular cerebellar histological layers were observed in the sham group, while EtOH induction caused loss of cerebellar tissue integrity, neuronal degeneration, vascular dilatation and congestion, reduced myelin density, and neuropils in the EtOH group. Zonisamide treatment improved these pathologies, enhancing myelination and neuropil formation. Negative APAF-1 and TNF-alpha expressions were observed across cerebellar layers in the sham group. Due to EtOH toxicity, APAF-1 and TNF-alpha expression were upregulated in the EtOH group compared to the sham group (p < 0.001 for both). Zonisamide treatment downregulated these protein expressions in the EtOH + zonisamide group compared to the EtOH group (p < 0.001 and p = 0.0087, respectively). APAF-1 was primarily associated with AA through antifolate resistance, endopeptidases, and the interleukin-1 pathway, while TNF-alpha was predominantly enriched in infections and choline-binding, indicating zonisamide's impact on immune and inflammatory pathways. In conclusion, zonisamide treatment significantly mitigated ethanol-induced cerebellar damage and inflammation in an AA model. Zonisamide improved locomotor function and reduced serum TNF-alpha levels, as well as APAF-1 and TNF-alpha expression in cerebellar tissues. These findings suggest that zonisamide exerts its protective effects by modulating immune and inflammatory pathways, thereby preserving cerebellar integrity and function.