Researcher:
Tosun, Yusuf Berk

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Undergraduate Student

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Yusuf Berk

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Tosun

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Tosun, Yusuf Berk

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2012 - 20132

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Researcher Of Publications: search.filters.isAuthorOfPublication.bd252038-2236-4c4a-a136-5b2fc88f94de

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    XENON in medical area: emphasis on neuroprotection in hypoxia and anesthesia
    (Wolters Kluwer Medknow Publications, 2013) Robinot, Alexander; Zhang, John H.; N/A; Esencan, Ecem; Yüksel, Simge; Tosun, Yusuf Berk; Solaroğlu, İhsan; Undergraduate Student; Undergraduated Student; Undergraduated Student; Faculty Member; School of Medicine; School of Medicine; School of Medicine; School of Medicine; Koç University Hospital; N/A; N/A; N/A; 102059
    Xenon is a medical gas capable of establishing neuroprotection, inducing anesthesia as well as serving in modern laser technology and nuclear medicine as a contrast agent. In spite of its high cost, its lack of side effects, safe cardiovascular and organoprotective profile and effective neuroprotective role after hypoxic-ischemic injury (HI) favor its applications in clinics. Xenon performs its anesthetic and neuroprotective functions through binding to glycine site of glutamatergic N-methyl-D-aspartate (NMDA) receptor competitively and blocking it. This blockage inhibits the overstimulation of NMDA receptors, thus preventing their following downstream calcium accumulating cascades. Xenon is also used in combination therapies together with hypothermia or sevoflurane. The neuroprotective effects of xenon and hypothermia cooperate synergistically whether they are applied synchronously or asynchronously. Distinguishing properties of Xenon promise for innovations in medical gas field once further studies are fulfilled and Xenon's high cost is overcome.
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    Early brain injury following aneurysmal. Subarachnoid hemorrhage: emphasis on cellular apoptosis
    (Turkish Neurosurgical Soc, 2012) Cahill, Julian; N/A; N/A; N/A; Yüksel, Simge; Tosun, Yusuf Berk; Solaroğlu, İhsan; Undergraduated Student; Undergraduate Student; Faculty Member; School of Medicine; School of Medicine; School of Medicine / RK-CTU; Koç University Hospital; N/A; N/A; 102059
    Subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture is a complex clinical disease with high mortality and morbidity. Recent studies suggest that early brain injury (EBI) rather than vasospasm might be responsible for morbidity and mortality within 24-72 hours after SAH. The rise in intracranial pressure following SAH causes a significant drop in cerebral perfusion press re that leads to global cerebral ischemia and initiates the acute injury cascade. Various molecular mechanisms have been shown to involve in the pathophysiology of EBI including cellular apoptosis. In this review, we summarize apoptotic molecular mechanisms involved in the etiology of EBI and its potential as a target for future therapeutic intervention.