@article{MTMT:34437579,
	title = {REPERFUSION FAILURE AFTER SPREADING DEPOLARIZATION SHAPES HEMOGLOBIN CONTENT IN THE MOUSE CORTEX},
	url = {https://m2.mtmt.hu/api/publication/34437579},
	author = {Törteli, Anna and Bálint, Armand Rafael and Tóth, Réka and Makra, Péter and Bari, Ferenc and Farkas, Eszter and Menyhárt, Ákos},
	doi = {10.1016/j.ibneur.2023.08.1306},
	journal-iso = {IBRO NEUROSCI REP},
	journal = {IBRO NEUROSCIENCE REPORTS},
	volume = {15},
	unique-id = {34437579},
	year = {2023},
	eissn = {2667-2421},
	pages = {S653-S653},
	orcid-numbers = {Makra, Péter/0000-0002-3213-6020; Farkas, Eszter/0000-0002-8478-9664; Menyhárt, Ákos/0000-0002-1355-3208}
}

@article{MTMT:34213830,
	title = {Nimodipine exerts a protective effect against spreading depolarization and neuroinflammation},
	url = {https://m2.mtmt.hu/api/publication/34213830},
	author = {Frank, Rita and Pesti, István and Menyhárt, Ákos and Szarvas, Péter and Gulya, Károly and Bari, Ferenc and Farkas, Eszter},
	doi = {10.1152/physiol.2023.38.S1.5762940},
	journal-iso = {PHYSIOLOGY},
	journal = {PHYSIOLOGY},
	volume = {38},
	unique-id = {34213830},
	issn = {1548-9213},
	abstract = {Hypothesis, objective: Voltage gated Ca2+ channels (VGCCs) are widely expressed in the central nervous system and implicated in neuronal injury and microglial activation. Nimodipine, a potent cerebrovascular dilator and VGCC antagonist is found to be effective against the vasoconstriction caused by spreading depolarization (SD) in preclinical studies of ischemia. However, it is still unclear whether the beneficial effect of nimodipine is achieved by the improvement of perfusion or a direct action on neuronal or glial cells. Our aim was to explore the direct action of nimodipine on the nervous tissue and microglia. Methods: Brain slices prepared from C57BL/6 mice (n=16) were perfused with artificial cerebrospinal fluid (aCSF). After 30 min nimodipine (nimo; 10 μM) incubation, low glucose aCSF (5 mM) and transient anoxia (1 min) were applied to mimic ischemia and to elicit SD. Intrinsic optical signal imaging was used to analyze SD features, TTC staining was applied to assess tissue injury. Primary mixed and pure microglia cultures prepared from the cortex of neonatal SPRD rats were treated with lipopolysaccharide (LPS;20 ng/ml) and nimodipine (5,10,20 μM), alone or in combination for 24 h. Microglial activation was evaluated by Iba1 immunolabeling (degree of arborization expressed by a transformation index (TI)), Western blot analysis and the visualization of phagocytosis with fluorescent microbeads. Results: In brain slices, nimodipine reduced the focal area of SD (2.37±0.94 vs 3.38±0.88%, nimo vs control), the total cortical area affected by SD (17.12±8.63 vs 39.88±22.42%, nimo vs control) and the propagation velocity of SD (0.19±0.79 vs 1.59±2.29mm/min, nimo vs control). Nimodipine decreased tissue injury, viability expressed as the number of TTC-stained particles (4.48±1.45 vs 3.52±1.52 particle/1000 μm2, nimo vs control). Nimodipine reduced microglial activation in LPS-treated cultures reflected by more ramified cell morphology (3.1±0.91 vs 1.89±0.41 TI, LPS+nimo vs LPS), decreased Iba1 intensity in Western blot analysis (108.3±20.1 and 77.2±8.49 vs 213.4±29.7 integrated optical density, LPS+nimo 10 and 20 μM vs LPS) and attenuated phagocytic activity (6±10 vs 22±20 bead/cell LPS+nimo vs LPS). Conclusion: Nimodipine was protective against SD and successfully reduced neuroinflammation by decreasing microglial activation. Neuroprotection was achieved independent of nimodipine’s vascular action. Our data suggest that nimodipine may be applicable against neuroinflammation and ischemia, in which neurodegeneration is believed to be linked to neurotoxic microglial activation.},
	year = {2023},
	eissn = {1548-9221},
	pages = {100-100},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:33803477,
	title = {Nimodipine augments cerebrovascular reactivity in aging but runs the risk of local perfusion reduction in acute cerebral ischemia},
	url = {https://m2.mtmt.hu/api/publication/33803477},
	author = {Kecskés, Szilvia and Menyhárt, Ákos and Bari, Ferenc and Farkas, Eszter},
	doi = {10.3389/fnagi.2023.1175281},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {15},
	unique-id = {33803477},
	issn = {1663-4365},
	year = {2023},
	eissn = {1663-4365},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:33691203,
	title = {Nimodipine accelerates the restoration of functional hyperemia during spreading oligemia},
	url = {https://m2.mtmt.hu/api/publication/33691203},
	author = {Menyhárt, Ákos and Bálint, Armand Rafael and Kozák, Péter and Bari, Ferenc and Farkas, Eszter},
	doi = {10.1111/jnc.15792},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	unique-id = {33691203},
	issn = {0022-3042},
	year = {2023},
	eissn = {1471-4159},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:33602905,
	title = {Spreading depolarization causes reperfusion failure after cerebral ischemia},
	url = {https://m2.mtmt.hu/api/publication/33602905},
	author = {Törteli, Anna and Tóth, Réka and Berger, Sarah and Samardzic, Sarah and Bari, Ferenc and Menyhárt, Ákos and Farkas, Eszter},
	doi = {10.1177/0271678X231153745},
	journal-iso = {J CEREBR BLOOD F MET},
	journal = {JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM},
	volume = {43},
	unique-id = {33602905},
	issn = {0271-678X},
	abstract = {Despite successful recanalization, reperfusion failure associated with poor neurological outcomes develops in half of treated stroke patients. We explore here whether spreading depolarization (SD) is a predictor of reperfusion failure. Global forebrain ischemia/reperfusion was induced in male and female C57BL/6 mice (n = 57). SD and cerebral blood flow (CBF) changes were visualized with transcranial intrinsic optical signal and laser speckle contrast imaging. To block SD, MK801 was applied (n = 26). Neurological deficit, circle of Willis (CoW) anatomy and neuronal injury were evaluated 24 hours later. SD emerged after ischemia onset in one or both hemispheres under a perfusion threshold (CBF drop to 21.1 ± 4.6 vs. 33.6 ± 4.4%, SD vs. no SD). The failure of later reperfusion (44.4 ± 12.5%) was invariably linked to previous SD. In contrast, reperfusion was adequate (98.9 ± 7.4%) in hemispheres devoid of SD. Absence of the P1 segment of the posterior cerebral artery in the CoW favored SD occurrence and reperfusion failure. SD occurrence and reperfusion failure were associated with poor neurologic function, and neuronal necrosis 24 hours after ischemia. The inhibition of SD significantly improved reperfusion. SD occurrence during ischemia impairs later reperfusion, prognosticating poor neurological outcomes. The increased likelihood of SD occurrence is predicted by inadequate collaterals.},
	keywords = {Reperfusion; ischemic stroke; Circle of Willis; Collaterals; Spreading depolarization},
	year = {2023},
	eissn = {1559-7016},
	pages = {655-664},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:34162729,
	title = {The inhibition of spreading depolarization may prevent reperfusion failure after ischemic stroke},
	url = {https://m2.mtmt.hu/api/publication/34162729},
	author = {Törteli, Anna and Tóth, Réka and Sarah, Samardzic and Sarah, Berger and Bari, Ferenc and Farkas, Eszter and Menyhárt, Ákos},
	journal-iso = {J CEREBR BLOOD F MET},
	journal = {JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM},
	volume = {42},
	unique-id = {34162729},
	issn = {0271-678X},
	abstract = {Background: Despite successful recanalization therapies (i.e., systemic thrombolysis, endovascular thrombectomy), insufficient reperfusion is often observed in ischemic stroke care. In fact, the efficiency of reperfusion might be determined by spreading depolarizations (SDs), secondary pathological events that trigger perfusion deficit and lesion maturation.
		Aim: Here, we aimed to improve reperfusion by the pharmacological blockade of SDs.
		Method: Male (n = 12) C57BL/6 mice were anesthetized with isoflurane (0.6–0.9%). A baseline of 10 min was followed by a transient (45 min) bilateral common carotid artery occlusion (2VO) and a subsequent 60 min reperfusion. Cerebral blood flow (CBF) variations were captured using green light reflectance and laser speckle contrast imaging. The irreversible NMDA receptor antagonist MK801 was applied intraperitoneally (0.3 mg/kg). Post stroke neurological deficit was classified after 24 hours on a Composite Garcia Neuroscore scale (0–21).
		Results/Conclusions: Low CBF early under ischemia favored SD evolution (SD vs. no SD; <25% vs. >35%). MK801 treatment reduced SD incidence (6/6 vs. 10/6 SD/animal; MK801 vs. Control) and the size of the cortical area invaded by SD (67.12 ± 11.3 vs. 85.32 ± 14.32%; MK801 vs. Control). In concert, MK801 improved the level of reperfusion (92.1 ± 12.37 vs. 54.5 ± 33.2%; MK801 vs. Control) and its slope (2.33 ± 0.78 vs. 0.78 ± 0.12%/s; MK801 vs. Control). Accordingly, MK801 treatment was associated with higher neuroscore values (18.33 ± 1.08 vs. 16.33 ± 0.57; MK801 vs. Control). Our data demonstrate that SD inhibition improves reperfusion after ischemic stroke. We propose that the pharmacological inhibition of SDs may facilitate sufficient reperfusion after recanalization in ischemic stroke care.},
	year = {2022},
	eissn = {1559-7016},
	pages = {151-151},
	orcid-numbers = {Farkas, Eszter/0000-0002-8478-9664; Menyhárt, Ákos/0000-0002-1355-3208}
}

@article{MTMT:34162683,
	title = {Spreading depolarization is implicated in insufficient reperfusion in the ischemic mouse cerebral cortex},
	url = {https://m2.mtmt.hu/api/publication/34162683},
	author = {Tóth, Réka and Törteli, Anna and Sarah, Berger and Sarah, Samardzic and Bari, Ferenc and Menyhárt, Ákos and Farkas, Eszter},
	journal-iso = {J CEREBR BLOOD F MET},
	journal = {JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM},
	volume = {42},
	unique-id = {34162683},
	issn = {0271-678X},
	abstract = {Background: Despite successful recanalization, reperfusion failure is often observed in ischemic stroke care. In fact, the efficiency of reperfusion might be determined by secondary pathophysiological events that evolve due to reduced collateral circulation in the ischemic brain. As the major principle of secondary brain injury, spreading depolarization (SD) triggers vasoconstriction and lesion maturation.
		Aim: We hypothesize that incomplete collateral anastomoses predict SD evolution under ischemia, which establishes reperfusion failure despite successful recanalization.
		Method: Male C57BL/6 mice (n = 15) were anesthetized with isoflurane (0.6–0.9%). After 10 min of baseline, transient (45 min) bilateral carotid artery occlusion (2VO) was followed by 60 min reperfusion. Intrinsic optical and cerebral blood flow (CBF) changes were captured using green light reflectance and laser speckle contrast imaging. Anatomical features of the circle of Willis were examined after carbon black ink perfusion.
		Results/Conclusions: Low CBF (<25%) during ischemia favored SD evolution (SD vs. no SD; <25% vs. >35%). SDs occurred in both hemispheres (bilateral) in 33%, in one hemisphere (unilateral) in 54% and in neither hemisphere (no-SD) in 13% of mice. In concert, reperfusion was insufficient in 33%, partial in 54%, and complete in 13% of the animals (28.74 ± 9.89 vs. 55.12 ± 13 vs. 96.88 ± 5.33% CBF, bilateral vs. unilateral vs. no SD). Accordingly, absence of the P1 segment of the posterior cerebral artery (PCA) was detected at the hemispheres affected by SD. Reperfusion failure is usually attributed to out-of-time intervention or localization of the infarct. We demonstrate that decreased collateral circulation fosters SD occurrence and insufficient reperfusion in ischemic stroke.},
	year = {2022},
	eissn = {1559-7016},
	pages = {150-151},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@book{MTMT:33267358,
	title = {Az egészségügyi informatika COVID előtt és COVID után - A XXXV. Neumann Kollokvium konferencia kiadványa},
	url = {https://m2.mtmt.hu/api/publication/33267358},
	isbn = {9786155036224},
	doi = {10.5281/zenodo.7376144},
	editor = {Bari, Ferenc and Rárosi, Ferenc and Szűcs, Mónika},
	publisher = {NJSZT},
	unique-id = {33267358},
	year = {2022},
	orcid-numbers = {Rárosi, Ferenc/0000-0002-1014-9242; Szűcs, Mónika/0000-0002-8791-9452}
}

@article{MTMT:32741246,
	title = {Biocompatible poly(ethylene succinate) polyester with molecular weight dependent drug release properties},
	url = {https://m2.mtmt.hu/api/publication/32741246},
	author = {Abdelghafour, Mohamed M. and Orbán, Ágoston and Imre-Deák, Ágota and Lamch, Łukasz and Nagyné Frank, Éva and Nagy, Roland and Ziegenheim, Szilveszter and Sipos, Pál Miklós and Farkas, Eszter and Bari, Ferenc and Janovák, László},
	doi = {10.1016/j.ijpharm.2022.121653},
	journal-iso = {INT J PHARM},
	journal = {INTERNATIONAL JOURNAL OF PHARMACEUTICS},
	volume = {618},
	unique-id = {32741246},
	issn = {0378-5173},
	year = {2022},
	eissn = {1873-3476},
	orcid-numbers = {Abdelghafour, Mohamed M./0000-0002-7895-4555; Imre-Deák, Ágota/0000-0002-6781-1727; Nagyné Frank, Éva/0000-0002-1332-0551; Sipos, Pál Miklós/0000-0003-1407-0950; Farkas, Eszter/0000-0002-8478-9664; Janovák, László/0000-0002-2066-319X}
}

@article{MTMT:32585588,
	title = {Transient Hypoperfusion to Ischemic/Anoxic Spreading Depolarization is Related to Autoregulatory Failure in the Rat Cerebral Cortex},
	url = {https://m2.mtmt.hu/api/publication/32585588},
	author = {Menyhárt, Ákos and Varga, Dániel Péter and M.Tóth, Orsolya and Makra, Péter and Bari, Ferenc and Farkas, Eszter},
	doi = {10.1007/s12028-021-01393-z},
	journal-iso = {NEUROCRIT CARE},
	journal = {NEUROCRITICAL CARE},
	volume = {37},
	unique-id = {32585588},
	issn = {1541-6933},
	year = {2022},
	eissn = {1556-0961},
	pages = {112-122},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Varga, Dániel Péter/0000-0001-5797-9334; Makra, Péter/0000-0002-3213-6020; Farkas, Eszter/0000-0002-8478-9664}
}