@article{MTMT:34824081,
	title = {Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches},
	url = {https://m2.mtmt.hu/api/publication/34824081},
	author = {Molnár, Tihamér and Lehoczki, Andrea Marianna and Fekete, Mónika and Várnai, Réka and Zavori, Laszlo and Erdő-Bonyár, Szabina and Simon, Diána and Berki, Tímea and Csécsei, Péter and Ezer, Erzsébet},
	doi = {10.1007/s11357-024-01165-5},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {In press},
	unique-id = {34824081},
	issn = {2509-2715},
	abstract = {The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has introduced the medical community to the phenomenon of long COVID, a condition characterized by persistent symptoms following the resolution of the acute phase of infection. Among the myriad of symptoms reported by long COVID sufferers, chronic fatigue, cognitive disturbances, and exercise intolerance are predominant, suggesting systemic alterations beyond the initial viral pathology. Emerging evidence has pointed to mitochondrial dysfunction as a potential underpinning mechanism contributing to the persistence and diversity of long COVID symptoms. This review aims to synthesize current findings related to mitochondrial dysfunction in long COVID, exploring its implications for cellular energy deficits, oxidative stress, immune dysregulation, metabolic disturbances, and endothelial dysfunction. Through a comprehensive analysis of the literature, we highlight the significance of mitochondrial health in the pathophysiology of long COVID, drawing parallels with similar clinical syndromes linked to post-infectious states in other diseases where mitochondrial impairment has been implicated. We discuss potential therapeutic strategies targeting mitochondrial function, including pharmacological interventions, lifestyle modifications, exercise, and dietary approaches, and emphasize the need for further research and collaborative efforts to advance our understanding and management of long COVID. This review underscores the critical role of mitochondrial dysfunction in long COVID and calls for a multidisciplinary approach to address the gaps in our knowledge and treatment options for those affected by this condition.},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Fekete, Mónika/0000-0001-8632-2120; Berki, Tímea/0000-0002-0134-8127}
}

@{MTMT:34823723,
	title = {A tromboembólia profilaxisa},
	url = {https://m2.mtmt.hu/api/publication/34823723},
	author = {Stankovics, Levente},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823723},
	year = {2024},
	pages = {170-171}
}

@{MTMT:34823698,
	title = {Agyödéma},
	url = {https://m2.mtmt.hu/api/publication/34823698},
	author = {Dóczi, Tamás Péter},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823698},
	year = {2024},
	pages = {67-74}
}

@{MTMT:34823697,
	title = {Az agyi neurobiomarkerek diagnosztikus és prognosztikus értéke},
	url = {https://m2.mtmt.hu/api/publication/34823697},
	author = {Czeiter, Endre and Amrein, Krisztina},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823697},
	year = {2024},
	pages = {63-66},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944}
}

@{MTMT:34823693,
	title = {Az agy véráramlásának autoregulációja},
	url = {https://m2.mtmt.hu/api/publication/34823693},
	author = {Tóth, Péter József},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823693},
	year = {2024},
	pages = {49-49}
}

@{MTMT:34823691,
	title = {Az agy keringésszabályozása},
	url = {https://m2.mtmt.hu/api/publication/34823691},
	author = {Tóth, Péter József},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823691},
	year = {2024},
	pages = {47-47}
}

@{MTMT:34823375,
	title = {Az agysérülés neuroanatómiája},
	url = {https://m2.mtmt.hu/api/publication/34823375},
	author = {Czeiter, Endre and Fazekas, Bálint and Amrein, Krisztina},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823375},
	year = {2024},
	pages = {33-46},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944; Fazekas, Bálint/0000-0002-8445-4100}
}

@article{MTMT:34804161,
	title = {Atherosclerotic burden and cerebral small vessel disease : exploring the link through microvascular aging and cerebral microhemorrhages},
	url = {https://m2.mtmt.hu/api/publication/34804161},
	author = {Csiszar, Anna and Ungvári, Anna Sára and Patai, Roland and Gulej, Rafal and Yabluchanskiy, Andriy and Benyó, Zoltán and Kovács, Illés and Sótonyi, Péter and Kirkpartrick, Angelia C and Prodan, Calin I and Liotta, Eric M and Zhang, Xin A and Tóth, Péter József and Tarantini, Stefano and Sorond, Farzaneh A and Ungvári, Zoltán István},
	doi = {10.1007/s11357-024-01139-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {in press},
	unique-id = {34804161},
	issn = {2509-2715},
	abstract = {Cerebral microhemorrhages (CMHs, also known as cerebral microbleeds) are a critical but frequently underestimated aspect of cerebral small vessel disease (CSVD), bearing substantial clinical consequences. Detectable through sensitive neuroimaging techniques, CMHs reveal an extensive pathological landscape. They are prevalent in the aging population, with multiple CMHs often being observed in a given individual. CMHs are closely associated with accelerated cognitive decline and are increasingly recognized as key contributors to the pathogenesis of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). This review paper delves into the hypothesis that atherosclerosis, a prevalent age-related large vessel disease, extends its pathological influence into the cerebral microcirculation, thereby contributing to the development and progression of CSVD, with a specific focus on CMHs. We explore the concept of vascular aging as a continuum, bridging macrovascular pathologies like atherosclerosis with microvascular abnormalities characteristic of CSVD. We posit that the same risk factors precipitating accelerated aging in large vessels (i.e., atherogenesis), primarily through oxidative stress and inflammatory pathways, similarly instigate accelerated microvascular aging. Accelerated microvascular aging leads to increased microvascular fragility, which in turn predisposes to the formation of CMHs. The presence of hypertension and amyloid pathology further intensifies this process. We comprehensively overview the current body of evidence supporting this interconnected vascular hypothesis. Our review includes an examination of epidemiological data, which provides insights into the prevalence and impact of CMHs in the context of atherosclerosis and CSVD. Furthermore, we explore the shared mechanisms between large vessel aging, atherogenesis, microvascular aging, and CSVD, particularly focusing on how these intertwined processes contribute to the genesis of CMHs. By highlighting the role of vascular aging in the pathophysiology of CMHs, this review seeks to enhance the understanding of CSVD and its links to systemic vascular disorders. Our aim is to provide insights that could inform future therapeutic approaches and research directions in the realm of neurovascular health.},
	keywords = {ATHEROSCLEROSIS; Aging; Blood-Brain Barrier; Arteriosclerosis; stroke; Leukoaraiosis; Peripheral artery disease; VASCULAR DEMENTIA; Microbleed; White matter hyperintensities; white matter injury},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Benyó, Zoltán/0000-0001-6015-0359; Kovács, Illés/0000-0001-5763-0482; Sótonyi, Péter/0000-0002-2216-4298; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@misc{MTMT:34794821,
	title = {Neural correlates of valence and arousal ratings responding to socio-emotional stimuli.},
	url = {https://m2.mtmt.hu/api/publication/34794821},
	author = {Rendes, Réka and Orsi, Gergely and Perlaki, Gábor and Bereczkei, Tamás and Deák, Anita},
	unique-id = {34794821},
	year = {2024},
	orcid-numbers = {Bereczkei, Tamás/0000-0002-4665-3475; Deák, Anita/0000-0001-6862-4993}
}

@{MTMT:34774903,
	title = {Additive manufacturing in limb prosthetics and orthotics: the past, present and future of 3D printing orthopedic assistive devices},
	url = {https://m2.mtmt.hu/api/publication/34774903},
	author = {Maróti, Péter and Schlégl, Ádám Tibor and Nagy, Bálint and Tóth, Luca and Bogár, Péter Zoltán and Józsa, Gergő and Rendeki, Szilárd and Mallakpour, Shadpour and Hussain, Chaudhery Mustansar},
	booktitle = {Medical Additive Manufacturing},
	doi = {10.1016/B978-0-323-95383-2.00028-7},
	unique-id = {34774903},
	year = {2024},
	pages = {179-207},
	orcid-numbers = {Maróti, Péter/0000-0001-7538-0675}
}