@article{MTMT:34803971,
	title = {Predictive factors of basic palliative and hospice care among patients with cancer visiting the emergency department in a Hungarian tertiary care center},
	url = {https://m2.mtmt.hu/api/publication/34803971},
	author = {Varga, Csaba and Springó, Zsolt and Koch, M. and Prenek, L. and Porcsa, L. and Bellyei, Szabolcs and Rumi, L. and Szabó, É. and Ungvári, Zoltán István and Girán, K. and Kiss, I. and Pozsgai, É.},
	doi = {10.1016/j.heliyon.2024.e29348},
	journal-iso = {HELIYON},
	journal = {HELIYON},
	volume = {10},
	unique-id = {34803971},
	year = {2024},
	eissn = {2405-8440},
	orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039}
}

@techreport{MTMT:32026751,
	title = {Az egészségügyi alapellátás és szolgáltatásainak fejlesztési lehetőségei a kistelepüléseken. Kutatási zárójelentés},
	url = {https://m2.mtmt.hu/api/publication/32026751},
	isbn = {9786158166409},
	author = {Roskovics, A and Springó, Zsolt and Barta, I and Batári, N and Mészáros, D and Zombai, Zs and Szabó, L},
	editor = {Szabó, Á and Kiss, Zs and Nagy, B},
	unique-id = {32026751},
	year = {2020}
}

@article{MTMT:30725481,
	title = {Chemically induced carcinogenesis in rodent models of aging: assessing organismal resilience to genotoxic stressors in geroscience research},
	url = {https://m2.mtmt.hu/api/publication/30725481},
	author = {Csiszar, Anna and Balasubramanian, Priya and Tarantini, Stefano and Yabluchanskiy, Andriy and Zhang, Xin A. and Springó, Zsolt and Benbrook, Doris and Sonntag, William E. and Ungvári, Zoltán István},
	doi = {10.1007/s11357-019-00064-4},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {41},
	unique-id = {30725481},
	issn = {2509-2715},
	abstract = {There is significant overlap between the cellular and molecular mechanisms of aging and pathways contributing to carcinogenesis, including the role of genome maintenance pathways. In the field of geroscience analysis of novel genetic mouse models with either a shortened, or an extended, lifespan provides a unique opportunity to evaluate the synergistic roles of longevity assurance pathways in cancer resistance and regulation of lifespan and to develop novel targets for interventions that both delay aging and prevent carcinogenesis. There is a growing need for robust assays to assess the susceptibility of cancer in these models. The present review focuses on a well-characterized method frequently used in cancer research, which can be adapted to study resilience to genotoxic stress and susceptibility to genotoxic stress-induced carcinogenesis in geroscience research namely, chemical carcinogenesis induced by treatment with 7,12-dimethylbenz(a)anthracene (DMBA). Recent progress in understanding how longer-living mice may achieve resistance to chemical carcinogenesis and how these pathways are modulated by anti-aging interventions is reviewed. Strain-specific differences in sensitivity to DMBA-induced carcinogenesis are also explored and contrasted with mouse lifespan. The clinical relevance of inhibition of DMBA-induced carcinogenesis for the pathogenesis of mammary adenocarcinomas in older human subjects is discussed. Finally, the potential role of insulin-like growth factor-1 (IGF-1) in the regulation of pathways responsible for cellular resilience to DMBA-induced mutagenesis is discussed.},
	keywords = {MUTATION; CANCER; TUMOR; CARCINOMA; MUTAGENESIS; DNA Repair; Health span},
	year = {2019},
	eissn = {2509-2723},
	pages = {209-227},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30452362,
	title = {IGF-1 Deficiency Exacerbates Hypertension-Induced Cerebral Microhemorrhages in Mice, Mimicking the Aging Phenotype},
	url = {https://m2.mtmt.hu/api/publication/30452362},
	author = {Tarantini, Stefano and Valcarcel-Ares, M. Noa and Yabluchanskiy, Andriy and Springó, Zsolt and Fulop, Gabor A. and Ungvári, Zoltán István},
	journal-iso = {J VASC RES},
	journal = {JOURNAL OF VASCULAR RESEARCH},
	volume = {54},
	unique-id = {30452362},
	issn = {1018-1172},
	keywords = {physiology},
	year = {2017},
	eissn = {1423-0135},
	pages = {25-26},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30452355,
	title = {Increased propensity for cerebral microhemorrhages in a IGF-1 deficient mouse model of accelerated vascular aging},
	url = {https://m2.mtmt.hu/api/publication/30452355},
	author = {Tarantini, Stefano and Valcarcel-Ares, Marta Noa and Yabluchanskiy, Andriy and Springó, Zsolt and Fülöp, Gábor Áron and Ashpole, Nicole and Gautam, Tripti and Giles, Cory and Wren, Jonathan D. and Sonntag, William E. and Csiszar, Anna and Ungvári, Zoltán István},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {31},
	unique-id = {30452355},
	issn = {0892-6638},
	keywords = {Biology; Biochemistry & Molecular Biology},
	year = {2017},
	eissn = {1530-6860},
	pages = {681.2-681.2},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:3331464,
	title = {Insulin-like growth factor 1 deficiency exacerbates hypertension-induced cerebral microhemorrhages in mice, mimicking the aging phenotype.},
	url = {https://m2.mtmt.hu/api/publication/3331464},
	author = {Tarantini, Stefano and Valcarcel-Ares, NM and Yabluchanskiy, A and Springó, Zsolt and Fülöp, Gábor Áron and Ashpole, N and Gautam, T and Giles, CB and Wren, JD and Sonntag, WE and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1111/acel.12583},
	journal-iso = {AGING CELL},
	journal = {AGING CELL},
	volume = {16},
	unique-id = {3331464},
	issn = {1474-9718},
	abstract = {Clinical and experimental studies show that aging exacerbates hypertension-induced cerebral microhemorrhages (CMHs), which progressively impair neuronal function. There is growing evidence that aging promotes insulin-like growth factor 1 (IGF-1) deficiency, which compromises multiple aspects of cerebromicrovascular and brain health. To determine the role of IGF-1 deficiency in the pathogenesis of CMHs, we induced hypertension in mice with liver-specific knockdown of IGF-1 (Igf1(f/f) + TBG-Cre-AAV8) and control mice by angiotensin II plus l-NAME treatment. In IGF-1-deficient mice, the same level of hypertension led to significantly earlier onset and increased incidence and neurological consequences of CMHs, as compared to control mice, as shown by neurological examination, gait analysis, and histological assessment of CMHs in serial brain sections. Previous studies showed that in aging, increased oxidative stress-mediated matrix metalloprotease (MMP) activation importantly contributes to the pathogenesis of CMHs. Thus, it is significant that hypertension-induced cerebrovascular oxidative stress and MMP activation were increased in IGF-1-deficient mice. We found that IGF-1 deficiency impaired hypertension-induced adaptive media hypertrophy and extracellular matrix remodeling, which together with the increased MMP activation likely also contributes to increased fragility of intracerebral arterioles. Collectively, IGF-1 deficiency promotes the pathogenesis of CMHs, mimicking the aging phenotype, which likely contribute to its deleterious effect on cognitive function. Therapeutic strategies that upregulate IGF-1 signaling in the cerebral vessels and/or reduce microvascular oxidative stress, and MMP activation may be useful for the prevention of CMHs, protecting cognitive function in high-risk elderly patients.},
	keywords = {Animals; Male; MICE; PHENOTYPE; Mice, Inbred C57BL; Psychomotor performance; Mice, Transgenic; Disease Models, Animal; Gait; Infusion Pumps, Implantable; Aging/*metabolism/pathology; Matrix Metalloproteinases/genetics/metabolism; Extracellular Matrix/*metabolism/pathology; NG-Nitroarginine Methyl Ester/administration & dosage; Insulin-Like Growth Factor I/*deficiency/genetics; Hypertension/chemically induced/complications/*metabolism/physiopathology; Cerebral Hemorrhage/chemically induced/etiology/*metabolism/physiopathology; Angiotensin II/administration & dosage; Oxidative stress},
	year = {2017},
	eissn = {1474-9726},
	pages = {469-479},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30452388,
	title = {IGF-1 Deficiency Exacerbates Hypertension-Induced Cerebral Microhemorrhages in Mice, Mimicking the Aging Phenotype},
	url = {https://m2.mtmt.hu/api/publication/30452388},
	author = {Tarantini, Stefano and Toth, Peter and Springó, Zsolt and Tucsek, Zsuzsanna and Valcarcel-Ares, Marta Noa and Gautam, Tripti and Sonntag, William and Csiszar, Anna and Ungvári, Zoltán István},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {29},
	unique-id = {30452388},
	issn = {0892-6638},
	keywords = {Biology; Biochemistry & Molecular Biology},
	year = {2015},
	eissn = {1530-6860},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:2798905,
	title = {Aging exacerbates hypertension-induced cerebral microhemorrhages in mice: role of resveratrol treatment in vasoprotection},
	url = {https://m2.mtmt.hu/api/publication/2798905},
	author = {Tóth, Péter József and Tarantini, Stefano and Springó, Zsolt and Tucsek, Z and Gautam, T and Giles, CB and Wren, JD and Koller, Ákos and Sonntag, WE and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1111/acel.12315},
	journal-iso = {AGING CELL},
	journal = {AGING CELL},
	volume = {14},
	unique-id = {2798905},
	issn = {1474-9718},
	abstract = {Recent studies demonstrate that aging exacerbates hypertension-induced cognitive decline, but the specific age-related mechanisms remain elusive. Cerebral microhemorrhages (CMHs) are associated with rupture of small intracerebral vessels and are thought to progressively impair neuronal function. To determine whether aging exacerbates hypertension-induced CMHs young (3months) and aged (24months) mice were treated with angiotensin II plus L-NAME. We found that the same level of hypertension leads to significantly earlier onset and increased incidence of CMHs in aged mice than in young mice, as shown by neurological examination, gait analysis, and histological assessment of CMHs in serial brain sections. Hypertension-induced cerebrovascular oxidative stress and redox-sensitive activation of matrix metalloproteinases (MMPs) were increased in aging. Treatment of aged mice with resveratrol significantly attenuated hypertension-induced oxidative stress, inhibited vascular MMP activation, significantly delayed the onset, and reduced the incidence of CMHs. Collectively, aging promotes CMHs in mice likely by exacerbating hypertension-induced oxidative stress and MMP activation. Therapeutic strategies that reduce microvascular oxidative stress and MMP activation may be useful for the prevention of CMHs, protecting neurocognitive function in high-risk elderly patients.},
	keywords = {ANGIOTENSIN-II; LIFE-SPAN; ACTIVATION; DEMENTIA; Cognitive function; NADPH OXIDASE; NADPH OXIDASE; endothelial function; Arteriole; CELL BIOLOGY; Microbleed; NAD(P)H OXIDASE; Microbleeds; MITOCHONDRIAL OXIDATIVE STRESS; Oxidative stress},
	year = {2015},
	eissn = {1474-9726},
	pages = {400-408},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Koller, Ákos/0000-0003-3256-8701; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:2798902,
	title = {Aging exacerbates pressure-induced mitochondrial oxidative stress in mouse cerebral arteries},
	url = {https://m2.mtmt.hu/api/publication/2798902},
	author = {Springó, Zsolt and Tarantini, Stefano and Tóth, Péter József and Tucsek, Z and Koller, Ákos and Sonntag, WE and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1093/gerona/glu244},
	journal-iso = {J GERONTOL A-BIOL MED SCI},
	journal = {JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES},
	volume = {70},
	unique-id = {2798902},
	issn = {1079-5006},
	abstract = {Epidemiological studies demonstrate that in addition to the increased prevalence of hypertension in old patients, the deleterious cerebrovascular effects of hypertension ( including atherosclerosis, stroke, and vascular cognitive impairment) are also exacerbated in elderly individuals. The cellular mechanisms by which aging and hypertension interact to promote cerebrovascular pathologies are not well understood. To test the hypothesis that aging exacerbates high pressure-induced mitochondrial oxidative stress, we exposed isolated segments of the middle cerebral arteries of young ( 3 months) and aged ( 24 months) C57BL/6 mice to 60 or 140 mmHg intraluminal pressure and assessed changes in mitochondrial reactive oxygen species production using a mitochondria-targeted redox-sensitive fluorescent indicator dye ( MitoSox) by confocal microscopy. Perinuclear MitoSox fluorescence was significantly stronger in high pressure-exposed middle cerebral arteries compared with middle cerebral arteries of the same animals exposed to 60 mmHg, indicating that high pressure increases mitochondrial reactive oxygen species production in the smooth muscle cells of cerebral arteries. Comparison of young and aged middle cerebral arteries showed that aging exacerbates high pressure-induced mitochondrial reactive oxygen species production in cerebral arteries. We propose that increased mechanosensitive mitochondrial oxidative stress may potentially exacerbate cerebrovascular injury and vascular inflammation in aging.},
	keywords = {ALZHEIMERS-DISEASE; HYPERTENSION; mitochondrion; SMOOTH-MUSCLE-CELLS; middle cerebral artery; Geriatrics & Gerontology; SECRETORY PHENOTYPE; NAD(P)H OXIDASE; CEREBROMICROVASCULAR ENDOTHELIAL-CELLS; IMPAIRS ANGIOGENIC CAPACITY; BETA-AMYLOID GENERATION; SUPEROXIDE-PRODUCTION; ACUTE HYPERTENSION; Oxidative stress},
	year = {2015},
	eissn = {1758-535X},
	pages = {1355-1359},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Koller, Ákos/0000-0003-3256-8701; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:2798900,
	title = {Aging impairs myogenic adaptation to pulsatile pressure in mouse cerebral Arteries},
	url = {https://m2.mtmt.hu/api/publication/2798900},
	author = {Springó, Zsolt and Tóth, Péter József and Tarantini, Stefano and Ashpole, M and Tucsek, Z and Sonntag, WE and Csiszar, Anna and Koller, Ákos and Ungvári, Zoltán István},
	doi = {10.1038/jcbfm.2014.256},
	journal-iso = {J CEREBR BLOOD F MET},
	journal = {JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM},
	volume = {35},
	unique-id = {2798900},
	issn = {0271-678X},
	abstract = {Stability of myogenic tone in middle cerebral arteries (MCA) is essential for adequate control over penetration of pressure waves into the distal portion of the cerebral microcirculation. Because the increased pulse pressure observed in advanced aging is associated with cerebromicrovascular injury, the effect of aging on myogenic response of mouse MCAs was determined. Aging did not affect the myogenic constriction in response to static increases in pressure, whereas it significantly impaired pulsatile pressure-induced myogenic tone. Impaired myogenic adaptation of MCAs to pulsatile pressure may allow high pressure to penetrate the distal portion of the cerebral microcirculation, contributing to microvascular damage.},
	keywords = {Brain; DISEASE; MICE; HYPERTENSION; Hematology; Hemodynamics; AUTOREGULATION; STIFFNESS; pulse wave; cerebral blood flow; PULSE-WAVE VELOCITY; Endocrinology & Metabolism},
	year = {2015},
	eissn = {1559-7016},
	pages = {527-530},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Koller, Ákos/0000-0003-3256-8701; Ungvári, Zoltán István/0000-0002-6035-6039}
}