TY - JOUR AU - Varga, Csaba AU - Springó, Zsolt AU - Koch, M. AU - Prenek, L. AU - Porcsa, L. AU - Bellyei, Szabolcs AU - Rumi, L. AU - Szabó, É. AU - Ungvári, Zoltán István AU - Girán, K. AU - Kiss, I. AU - Pozsgai, É. TI - Predictive factors of basic palliative and hospice care among patients with cancer visiting the emergency department in a Hungarian tertiary care center JF - HELIYON J2 - HELIYON VL - 10 PY - 2024 IS - 8 PG - 11 SN - 2405-8440 DO - 10.1016/j.heliyon.2024.e29348 UR - https://m2.mtmt.hu/api/publication/34803971 ID - 34803971 LA - English DB - MTMT ER - TY - GEN ED - Szabó, Á ED - Kiss, Zs ED - Nagy, B AU - Roskovics, A AU - Springó, Zsolt AU - Barta, I AU - Batári, N AU - Mészáros, D AU - Zombai, Zs AU - Szabó, L TI - Az egészségügyi alapellátás és szolgáltatásainak fejlesztési lehetőségei a kistelepüléseken. Kutatási zárójelentés TS - Kutatási zárójelentés PY - 2020 SN - 9786158166409 UR - https://m2.mtmt.hu/api/publication/32026751 ID - 32026751 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Csiszar, Anna AU - Balasubramanian, Priya AU - Tarantini, Stefano AU - Yabluchanskiy, Andriy AU - Zhang, Xin A. AU - Springó, Zsolt AU - Benbrook, Doris AU - Sonntag, William E. AU - Ungvári, Zoltán István TI - Chemically induced carcinogenesis in rodent models of aging: assessing organismal resilience to genotoxic stressors in geroscience research JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 41 PY - 2019 IS - 2 SP - 209 EP - 227 PG - 19 SN - 2509-2715 DO - 10.1007/s11357-019-00064-4 UR - https://m2.mtmt.hu/api/publication/30725481 ID - 30725481 N1 - Funding Agency and Grant Number: American Heart Association; National Institute on Aging [R01-AG055395, R01-AG047879, R01-AG038747]; National Heart Lung Blood Institute [R01HL132553]; National Institute of Neurological Disorders and Stroke (NINDS) [R01-NS056218, R01-NS100782]; NIA [T32AG052363, 3P30AG050911-02S1]; NIH [NIGMS U54GM104938]; National Cancer Institute [R01-CA196200, R01-CA200126]; Oklahoma Center for the Advancement of Science and Technology; Presbyterian Health Foundation; Reynolds Foundation Funding text: This work was supported by grants from the American Heart Association (to ST), the National Institute on Aging (R01-AG055395 to ZU, R01-AG047879 to AC, R01-AG038747), the National Heart Lung Blood Institute (R01HL132553), the National Institute of Neurological Disorders and Stroke (NINDS; R01-NS056218 to AC, R01-NS100782 to ZU), the NIA-supported Geroscience Training Program in Oklahoma (T32AG052363), the NIA-supported Oklahoma Nathan Shock Center (to ZU and AC; 3P30AG050911-02S1), NIH-supported Oklahoma Shared Clinical and Translational Resources (to AY, NIGMS U54GM104938), the National Cancer Institute (R01-CA196200 and R01-CA200126 to DMB), the Oklahoma Center for the Advancement of Science and Technology (to AC, ZU, AY), the Presbyterian Health Foundation (to ZU, AC, AY), and the Reynolds Foundation (to ZU and AC). AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Tarantini, Stefano AU - Valcarcel-Ares, M. Noa AU - Yabluchanskiy, Andriy AU - Springó, Zsolt AU - Fulop, Gabor A. AU - Ungvári, Zoltán István TI - IGF-1 Deficiency Exacerbates Hypertension-Induced Cerebral Microhemorrhages in Mice, Mimicking the Aging Phenotype JF - JOURNAL OF VASCULAR RESEARCH J2 - J VASC RES VL - 54 PY - 2017 SP - 25 EP - 26 PG - 2 SN - 1018-1172 UR - https://m2.mtmt.hu/api/publication/30452362 ID - 30452362 LA - English DB - MTMT ER - TY - JOUR AU - Tarantini, Stefano AU - Valcarcel-Ares, Marta Noa AU - Yabluchanskiy, Andriy AU - Springó, Zsolt AU - Fülöp, Gábor Áron AU - Ashpole, Nicole AU - Gautam, Tripti AU - Giles, Cory AU - Wren, Jonathan D. AU - Sonntag, William E. AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Increased propensity for cerebral microhemorrhages in a IGF-1 deficient mouse model of accelerated vascular aging JF - FASEB JOURNAL J2 - FASEB J VL - 31 PY - 2017 IS - S1 SP - 681.2 EP - 681.2 PG - 1 SN - 0892-6638 UR - https://m2.mtmt.hu/api/publication/30452355 ID - 30452355 LA - English DB - MTMT ER - TY - JOUR AU - Tarantini, Stefano AU - Valcarcel-Ares, NM AU - Yabluchanskiy, A AU - Springó, Zsolt AU - Fülöp, Gábor Áron AU - Ashpole, N AU - Gautam, T AU - Giles, CB AU - Wren, JD AU - Sonntag, WE AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Insulin-like growth factor 1 deficiency exacerbates hypertension-induced cerebral microhemorrhages in mice, mimicking the aging phenotype. JF - AGING CELL J2 - AGING CELL VL - 16 PY - 2017 IS - 3 SP - 469 EP - 479 PG - 11 SN - 1474-9718 DO - 10.1111/acel.12583 UR - https://m2.mtmt.hu/api/publication/3331464 ID - 3331464 N1 - * Megosztott szerzőség AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Tarantini, Stefano AU - Toth, Peter AU - Springó, Zsolt AU - Tucsek, Zsuzsanna AU - Valcarcel-Ares, Marta Noa AU - Gautam, Tripti AU - Sonntag, William AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - IGF-1 Deficiency Exacerbates Hypertension-Induced Cerebral Microhemorrhages in Mice, Mimicking the Aging Phenotype JF - FASEB JOURNAL J2 - FASEB J VL - 29 PY - 2015 IS - S1 PG - 1 SN - 0892-6638 UR - https://m2.mtmt.hu/api/publication/30452388 ID - 30452388 LA - English DB - MTMT ER - TY - JOUR AU - Tóth, Péter József AU - Tarantini, Stefano AU - Springó, Zsolt AU - Tucsek, Z AU - Gautam, T AU - Giles, CB AU - Wren, JD AU - Koller, Ákos AU - Sonntag, WE AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Aging exacerbates hypertension-induced cerebral microhemorrhages in mice: role of resveratrol treatment in vasoprotection JF - AGING CELL J2 - AGING CELL VL - 14 PY - 2015 IS - 3 SP - 400 EP - 408 PG - 9 SN - 1474-9718 DO - 10.1111/acel.12315 UR - https://m2.mtmt.hu/api/publication/2798905 ID - 2798905 N1 - * Megosztott szerzőség AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Springó, Zsolt AU - Tarantini, Stefano AU - Tóth, Péter József AU - Tucsek, Z AU - Koller, Ákos AU - Sonntag, WE AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Aging exacerbates pressure-induced mitochondrial oxidative stress in mouse cerebral arteries JF - JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES J2 - J GERONTOL A-BIOL MED SCI VL - 70 PY - 2015 IS - 11 SP - 1355 EP - 1359 PG - 5 SN - 1079-5006 DO - 10.1093/gerona/glu244 UR - https://m2.mtmt.hu/api/publication/2798902 ID - 2798902 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Springó, Zsolt AU - Tóth, Péter József AU - Tarantini, Stefano AU - Ashpole, M AU - Tucsek, Z AU - Sonntag, WE AU - Csiszar, Anna AU - Koller, Ákos AU - Ungvári, Zoltán István TI - Aging impairs myogenic adaptation to pulsatile pressure in mouse cerebral Arteries JF - JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM J2 - J CEREBR BLOOD F MET VL - 35 PY - 2015 IS - 4 SP - 527 EP - 530 PG - 4 SN - 0271-678X DO - 10.1038/jcbfm.2014.256 UR - https://m2.mtmt.hu/api/publication/2798900 ID - 2798900 N1 - * Megosztott szerzőség AB - 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. LA - English DB - MTMT ER -