Ertener, Özge

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https://hdl.handle.net/20.500.14365/6934
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Ertener, Ozge
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Email Address
ozge.cokbankir@ieu.edu.tr
Main Affiliation
09.04. Surgical Sciences
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Current Staff
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0000-0002-4957-7877
Scopus Author ID
55851481300
Turkish CoHE Profile ID
157D539DE7A82428
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WoS Researcher ID
EUA-8492-2022
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Ozge_Ertener.png (62.76 KB)

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Eurasıan Journal of Emergency Medıcıne1
INJURY-International Journal of the Care of the Injured1
Kuwaıt Medıcal Journal1
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  • Thumbnail Image
    Article
    Ipsilateral Synchronous Renal Cell Carcinoma: Papillary and Chromophobe
    (Kuwait Medical Assoc, 2022) Adali, Yasemen; Toyran, Tugba; Ertener, Ozge
    Synchronous renal tumors are the general name of multiple tumors with bilateral or unilateral location which are less frequently seen. Here, we present a case of papillary renal cell carcinoma (pRCC) and chromophobe renal cell carcinoma (chRCC) as a rare entity in a single kidney. A 41-year-old woman underwent a radical nephrectomy for a mass with an 11 cm diameter localized in the lower left pole. Macroscopic examination revealed a 10.5x9.5 cm sized tumor and one more tumor 1 cm away from this tumor sized 1.7x1.2 cm. The histopathological and immunohistochemical features of the two tumors were evaluated and were diagnosed as chRCC and pRCC. Synchronous renal tumors are rare. Generally one component of renal synchronous tumors reported in the literature is usually clear cell renal cell carcinoma, which is the most frequently seen renal cell carcinoma type of all. We present this case because of it's uniqueness.
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    Article
    Effects of Varenicline as an Adjunct to Analgesic and Anti-Inflammatory Therapy in Acute Nerve Injury
    (Elsevier Sci Ltd, 2026) Ozturk, Volga; Rusen, Yasemen Adali; Ertener, Ozge; Seval-Celik, Yasemin; Dastan, Ali Engin; Ozgenc, Serhat; Baris, Elif
    Introduction: Acute nerve injury (ANI) leads to significant neuropathic pain and functional impairment. Current treatments, including nonsteroidal anti-inflammatory drugs (NSAIDs) like meloxicam, provide symptomatic relief but have limited neuroregenerative effects. Varenicline, a nicotinic acetylcholine receptor (nAChR) agonist, has demonstrated neuroprotective and anti-inflammatory properties. Aim: This study evaluates the effects of varenicline as an add-on therapy to meloxicam in a rat model of ANI. Methods: Eighteen female Wistar rats were randomized into four groups: Control (CONT), Sham (SHAM), Acute Nerve Injury + Meloxicam (ANI+Melox), and Acute Nerve Injury + Meloxicam + Varenicline (ANI+Melox+VAR). Varenicline (2.5 mg/kg, s.c.) was administered alongside meloxicam (2 mg/kg, s.c.). Functional recovery, histopathological changes, and biochemical markers, including prostaglandins (PGE2, PGI2), substance P, IL-6, levels, were assessed after 30 days. Results: Varenicline and meloxicam co-treatment significantly reduced inflammatory and pain biomarkers including prostaglandins, interleukin-6 and substance P, compared to meloxicam alone. Histopathological evaluation revealed enhanced Schwann cell proliferation, reduced fibrosis, and increased Bands of B & uuml;ngner formation, suggesting nerve regeneration. Conclusion: Varenicline, as an adjunct to meloxicam, enhances neuroprotection, reduces inflammation, and promotes histological and biochemical indicators of regeneration in rats with acute sciatic nerve injury. Future studies should explore its long-term effects and potential as a monotherapy for peripheral nerve injuries.
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    Article
    Can Spesific Biomarkers Be Used To Enlighten the Major Mechanisms of Acute High Dose Diclofenac Sodium-Related Nephrotoxicity?
    (Galenos Publ House, 2022) Dogruyol, Sinem; Akbas, Ilker; Kocak, Abdullah Osman; Aygormez, Serpil; Leylek, Habip Emrah; Gur, Sultan Tuna Akgol; Ertener, Ozge
    Aim: The aim of this study was to examine the basic mechanisms that play a role in the acute nephrotoxicity caused by diclofenac sodium. Materials and Methods: Only water was given to the control group; however, the diclofenac sodium group was group intoxicated by giving water-soluble, 240 mg/kg, oral single dose diclofenac sodium. After 24 hours, all animals were sacrificed and histopathological analyzes were performed. The levels of spesific biomarkers [vascular endothelial growth factor (VEGF), nuclear factor-kappa B (NF-kappa B), matrix metalloproteinase-9 (MMP-9), metalloproteinase tissue inhibitor-1 (TIMP-1) and carcinoembryonic antigen (CEA)] that may be related to the nephrotoxicity mechanism were evaluated. Results: As a result of biochemical analysis, we found that VEGF, TIMP-1, NF-kappa B and CEA levels were significantly higher and MMP-9 levels were significantly lower in diclofenac sodium group compared to control group. Nephrotoxicity related histopathological changes were observed in the sections of diclofenac sodium group. Conclusion: This study has shown that the biomarkers we evaluated in the diclofenac sodium-induced acute high-dose intoxication model we created can help us to identify the nephrotoxicity and to explain the nephrotoxicity mechanism with the three main steps (the hemodynamicrelated pathway, the inflammation-related pathway, and the oxidative stress-related pathway). With a simple version of this panel adapted to emergency departments, we may be able to diagnose diclofenac sodium-related nephrotoxicity.