Ender Erdoğan

Prof. Dr. Ender Erdoğan

orcid

Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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24 September 2018 in Scientific Reports
Verified
Journal Article
Open access
PDF file
MAMehmet Şerif Aydın
Mehmet Şerif Aydın
EYEsra Nur Yiğit
Esra Nur Yiğit
EVEmre Vatandaşlar
Emre Vatandaşlar
EEEnder Erdoğan
Ender Erdoğan
GOGurkan Ozturk
Gurkan Ozturk
Beside its unique nutritional content breast milk also contains live cells from the mother. Fate of these cells in the offspring has not been adequately described. In this study, we aimed to detect and identify maternal cells in the suckling’s blood and the brain. Green fluorescent protein expressing transgenic female mice (GFP+) were used as foster mothers to breastfeed wildtype newborn pups. One week and two months after the birth, blood samples and brains of the sucklings were analyzed to detect presence of GFP+ cells by fluorescence activated cell sorting, polymerase chain reaction and immunohistochemistry on the brain sections and optically cleared brains. The tests confirmed that maternal cells were detectable in the blood and the brain of the pups and that they differentiated into both neuronal and glial cell types in the brain. This phenomenon represents breastfeeding – induced microchimerism in the brain with functional implications remain to be understood.

5 March 2017 in Artificial Organs
Verified
Journal Article
Closed access
PDF file
MOMerih Onal
Merih Onal
CECagdas Elsurer
Cagdas Elsurer
NSNebil Selimoglu
Nebil Selimoglu
MYMustafa Yilmaz
Mustafa Yilmaz
EEEnder Erdoğan
Ender Erdoğan
OOOzkan Onal
Ozkan Onal

5 November 2016 in Brazilian Journal of Otorhinolaryngology
Verified
Journal Article
Open access
MÇMetin Çeliker
Metin Çeliker
AÖAbdulkadir Özgür
Abdulkadir Özgür
LTLevent Tümkaya
Levent Tümkaya
STSuat Terzi
Suat Terzi
MYMustafa Yılmaz
Mustafa Yılmaz
EEEnder Erdoğan
Ender Erdoğan
The use of mobile phones has become widespread in recent years. Although beneficial from the communication viewpoint, the electromagnetic fields generated by mobile phones may cause unwanted biological changes in the human body. In this study, we aimed to evaluate the effects of 2100MHz Global System for Mobile communication (GSM-like) electromagnetic field, generated by an electromagnetic fields generator, on the auditory system of rats by using electrophysiological, histopathologic and immunohistochemical methods. Fourteen adult Wistar albino rats were included in the study. The rats were divided randomly into two groups of seven rats each. The study group was exposed continuously for 30days to a 2100MHz electromagnetic fields with a signal level (power) of 5.4dBm (3.47mW) to simulate the talk mode on a mobile phone. The control group was not exposed to the aforementioned electromagnetic fields. After 30days, the Auditory Brainstem Responses of both groups were recorded and the rats were sacrificed. The cochlear nuclei were evaluated by histopathologic and immunohistochemical methods. The Auditory Brainstem Responses records of the two groups did not differ significantly. The histopathologic analysis showed increased degeneration signs in the study group (p=0.007). In addition, immunohistochemical analysis revealed increased apoptotic index in the study group compared to that in the control group (p=0.002). The results support that long-term exposure to a GSM-like 2100MHz electromagnetic fields causes an increase in neuronal degeneration and apoptosis in the auditory system.

9 September 2021 in Advances in Clinical and Experimental Medicine
Verified
Journal Article
Open access
ZGZahide Gunduz
Zahide Gunduz
FAFiliz Aktas
Filiz Aktas
HVHüsamettin Vatansev
Hüsamettin Vatansev
MSMerve Solmaz
Merve Solmaz
EEEnder Erdoğan
Ender Erdoğan
Ischemia-reperfusion models are used to evaluate treatment options that may minimize cellular damage after ischemia. To investigate the effects of amantadine and topiramate on apoptosis and cellular oxidative damage. This experiment was performed using 30 male Wistar albino rats. The right internal carotid artery was identified and clamped with an aneurysm clip under general anesthesia, except for animals in the control group. After 10 min of occlusion, the aneurysm clip was removed, allowing reperfusion. After reperfusion and a waiting period of 12 h, the test and control groups were intraperitoneally administered the following solutions: the sham group received 10 mg/kg of isotonic solution, the amantadine group received 20 mg/kg of amantadine, the topiramate group received 40 mg/kg of topiramate, and the amantadine-topiramate group received 20 mg/kg of amantadine and 40 mg/kg of topiramate. After 24 h, the rats were euthanized. Apoptosis was evaluated using the TUNEL method. Total antioxidant status (TAS), total oxidant status (TOS), total thiol, and ischemia-modified albumin (IMA) levels were measured in both brain tissue and serum samples. The rate of apoptosis in the sham and amantadine groups increased significantly compared to the control group and the non-ischemic counter hemisphere. In the amantadine-topiramate group, both serum TAS and tissue thiol levels decreased. Tissue TOS levels were significantly higher in the topiramate group compared to all other test groups. Tissue TAS levels were significantly higher in the amantadine group compared to all other test groups. This experimental ischemia-reperfusion model revealed that topiramate reduces apoptosis in the early period after ischemia and that its combination with amantadine does not provide additional benefits against cell death. However, topiramate did not have an inhibitory effect on the oxidative stress biomarkers used in our study (TAS, TOS, IMA, and thiol). Studies that reveal the neuroprotective mechanism of action and long-term effects of topiramate are needed to complement this study.

19 October 2018 in Journal of Investigative Surgery
Verified
Journal Article
Closed access
CECagdas Elsurer
Cagdas Elsurer
MOMerih Onal
Merih Onal
NSNebil Selimoglu
Nebil Selimoglu
OEOmer Erdur
Omer Erdur
MYMustafa Yilmaz
Mustafa Yilmaz
OOOzkan Onal
Ozkan Onal
Introduction: Muscle-flap transferring is a routine approach utilized in reconstructive operations; however, flap morbidity is often a source of post-operative difficulty. Ischemia-Reperfusion Injury (IRI) is an important contributor to the viability of flaps after transferring. The goal of this research was for assess the probable useful impacts of ozone on flap survival in a rat muscle-flap design. Materials and Methods: We examined the effects of postconditioning ozone administration on viability of pedicled composite flaps. Twenty-eight Wistar rats were randomized into four groups: sham-operated (S), ischemia-reperfusion (IR), sham-operated + ozone (O), IR + ozone (IR + O), respectively. The animals were sacrificed on the eighth day. In a general histological evaluation, flap tissues were examined with a light microscope, and apoptotic cells were counted. The Apoptotic Index (AI) was then calculated. Flap-tissue samples were sent for analyses of malondialdehyde (MDA), catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and protein carbonyl (PCO), and blood samples were sent for analyses of Total Oxidant Score (TOS), and Total Antioxidant Capacity (TAC). Data were evaluated statistically using the Kruskal–Wallis test. Results: The histomorphometric score was remarkably greater in O (p = .002). The AI was greater in IR (p = .002). The antioxidant parameters values as regards SOD, GSH-Px, CAT, and TAC were found to be greater in O (p < .005). The oxidant parameters values as regards MDA, PCO, TOS were found to be greater in IR (p < .005). Discussion: The current research indicates that ozone application can attenuate the muscle-flap injury brought about by IR through triggering the increase of the antioxidant capacity.

25 May 2026 in Anatomia, Histologia, Embryologia
Verified
Journal Article
Closed access
INIsmail Hakki NUR
Ismail Hakki NUR
WILLIAM PÉREZWILLIAM PÉREZ
WILLIAM PÉREZ
CRCatrin Sian Rutland
Catrin Sian Rutland
HKHorst Erich König
Horst Erich König
NÜNejat Ünlükal
Nejat Ünlükal
EEEnder Erdoğan
Ender Erdoğan