Seher Yilmaz

Dr. Seher Yilmaz


Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

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

Representative Publications

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1 January 2022 in Folia Neuropathologica
Verified
Journal Article
Open access
PDF file
GKGulnara Kapanova
Gulnara Kapanova
GTGulnara Tashenova
Gulnara Tashenova
AAAida Akhenbekova
Aida Akhenbekova
ATAdem Tokpınar
Adem Tokpınar
SYSeher Yilmaz
Seher Yilmaz
Cerebral ischemia/reperfusion injury has emerged as an intricate mechanism. However, identification of wide-ranging mechanisms which mechanistically regulate reperfusion injuries have significantly improved our understanding. Recent advancements in our knowledge about the molecular consequences...

8 May 2020 in Biomedicines
Verified
Journal Article
Open access
PDF file
Enes AkyuzEnes Akyuz
Enes Akyuz
ZDZüleyha Doğanyiğit
Züleyha Doğanyiğit
Yam Nath PaudelYam Nath Paudel
Yam Nath Paudel
EKEmin Kaymak
Emin Kaymak
SYSeher Yilmaz
Seher Yilmaz
Mohmad Farooq ShaikhMohmad Farooq Shaikh
Mohmad Farooq Shaikh
Experimental and clinical studies of cardiac pathology associated with epilepsy have demonstrated an impact on the autonomic nervous system (ANS). However, the underlying molecular mechanism has not been fully elucidated. Molecular investigation of the neurotransmitters related receptor and ion channel directing ANS might help in understanding the associated mechanism. In this paper, we investigated the role of acetylcholine (ACh), which demonstrates both sympathetic and parasympathetic roles in targeted expression in terms of the relevant receptor and ion channel. Inwardly rectifying potassium (Kir) channels play a significant role in maintaining the resting membrane potential and controlling cell excitability and are prominently expressed in both the excitable and non-excitable tissues. The immunoreactivity of ACh-activated Kir3.1 channel and muscarinic ACh receptors (M2) in autonomic centers such as the brainstem, vagus nerve (VN) and atria of heart was confirmed by both histological staining and pathological tissue analysis. Significant upregulations of Kir3.1 and M2 receptors were observed in pentylenetetrazol (PTZ)-kindled epileptic rats for all related tissues investigated, whereas no pathological difference was observed. These findings provide proof-of-concept that changes in ACh-associated immunoreactivity might be linked to the ANS dysfunctions associated with epilepsy.

9 June 2020 in Diagnostics
Verified
Journal Article
Open access
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Enes AkyuzEnes Akyuz
Enes Akyuz
KPKristina Polat
Kristina Polat
ŞAŞükrü Ateş
Şükrü Ateş
DUDemet Unalmis
Demet Unalmis
ATAdem Tokpınar
Adem Tokpınar
Chiara VillaChiara Villa
Chiara Villa
Epilepsy is a group of neurological disorders characterized by abnormal electrical activity in the central nervous system (CNS) and recurrent seizures representing the principal clinical manifestation. Sudden unexpected death in epilepsy (SUDEP) is the predominant cause of death in young epileptic patients. SUDEP patients displayed an increased cardiovascular (CV) risk, probably due to an impaired autonomic control of CV functions, but the underlying mechanisms need to be explored yet. Therefore, we aimed to examine the cardiac morphological alterations in a pentylenetetrazol (PTZ)-kindled rat model, a well-established tool for studying chronic epilepsy. To complete this, the distance between the atria, between the atrium and ventricle were measured, the heart was weighed, and the pathological morphology of dissected hearts was analyzed by histological assessment with hematoxylin and eosin staining. A significantly decreased distance between atria and a significant increase in heart weight were observed in PTZ-kindled rats which interestingly also displayed increased hemorrhagic content when compared with controls. Our findings provided evidence that changes in cardiac morphology may be related to autonomic CV dysfunctions occurring during SUDEP while also opening up more avenues to better develop novel drugs for the treatment of this disorder.

27 March 2023 in Cell Biochemistry and Function
Verified
Journal Article
Closed access
AOAslı Okan
Aslı Okan
ZDZüleyha Doğanyiğit
Züleyha Doğanyiğit
SYSeher Yilmaz
Seher Yilmaz
SUSümeyye Uçar
Sümeyye Uçar
ESEvrim Suna Arikan Söylemez
Evrim Suna Arikan Söylemez
RARukset Attar
Rukset Attar

27 March 2023 in Medical Oncology
Verified
Journal Article
Closed access
PDF file
SYSeher Yilmaz
Seher Yilmaz
ZDZüleyha Doğanyiğit
Züleyha Doğanyiğit
AOAslı Okan Oflamaz
Aslı Okan Oflamaz
ŞAŞükrü Ateş
Şükrü Ateş
ESEvrim Suna Arıkan Söylemez
Evrim Suna Arıkan Söylemez
AFAmmad Farooqi
Ammad Farooqi

1 September 2020 in Asian Pacific Journal of Cancer Prevention
Verified
Journal Article
Open access
PDF file
SYSeher Yilmaz
Seher Yilmaz
AGAyşe Yeşim Göçmen
Ayşe Yeşim Göçmen
EKErsin Karataş
Ersin Karataş
ATAdem Tokpınar
Adem Tokpınar
Cornelian Cherry (Cornus Mas L) has widespread use due to its anti-inflammatory, anti-carcinogenic and anti-oxidant properties. In this study, the effects of Cornus Mas L (C. mas L) in different dosages on the biochemical values of mice organs were investigated in the Ehrlich Ascites tumor model, which originated from mice breast adenocarcinoma and developed in Balb/C mice. In our study, 32 Balb/C type male mice were used. Ehrlich Ascites Tumor (EAT) cells (1x106 EAT cell) from the stock animal were injected into all the mice in an intraperitoneal way. Experimental groups were given 100 and 200mg/kg C. mas L extract intraperitoneally for 9 days. The weights of the animals were recorded every day and were sacrificed on the 9th day. To estimate tumor proliferation of the lung, brain, kidney, liver, and testis, antioxidant parameters were recorded including, the reduced glutathione (GSH), lipid peroxidation, glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT). Treatments of different doses of C. mas L. meaningfully (p < 0.05) modulated the lung, brain, kidney, liver and testis tissues antioxidant parameters as compared to the control. Our study showed the anti-tumor effect of C. mas L. in assisted tumor development with EAT cells, conceivably moderated by the enhancement of oxidative stress due to numerous mechanisms.