TY - JOUR AU - Szarvas, Zsófia AU - Fekete, Mónika AU - Szőllősi, Gergő József AU - Kup, Katica Anna AU - Horvath, Rita AU - Shimizu, Maya AU - Tsuhiya, Fuko AU - Choi, Ha Eun AU - Wu, Huang-Tzu AU - Fazekas-Pongor, Vince AU - Pete, Kinga Nedda AU - Cserjesi, Renata AU - Bakos, Regina AU - Gőbel, Orsolya AU - Gyongyosi, Kata AU - Pinter, Renata AU - Kolozsvari, Dora AU - Jáky-Kováts, Zsuzsanna Ágnes AU - Yabluchanskiy, Andriy AU - Owens, Cameron D. AU - Ungvári, Zoltán István AU - Tarantini, Stefano AU - Horváth, Gábor AU - Müller, Veronika AU - Varga, János Tamás TI - Optimizing cardiopulmonary rehabilitation duration for long COVID patients: an exercise physiology monitoring approach JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - in press PY - 2024 SP - in press SN - 2509-2715 DO - 10.1007/s11357-024-01179-z UR - https://m2.mtmt.hu/api/publication/34866258 ID - 34866258 AB - The presence of prolonged symptoms after COVID infection worsens the workability and quality of life. 200 adults with long COVID syndrome were enrolled after medical, physical, and mental screening, and were divided into two groups based on their performance. The intervention group ( n = 100) received supervised rehabilitation at Department of Pulmonology, Semmelweis University with the registration number 160/2021 between 01/APR/2021–31/DEC/2022, while an age-matched control group ( n = 100) received a single check-up. To evaluate the long-term effects of the rehabilitation, the intervention group was involved in a 2- and 3-month follow-up, carrying out cardiopulmonary exercise test. Our study contributes understanding long COVID rehabilitation, emphasizing the potential benefits of structured cardiopulmonary rehabilitation in enhancing patient outcomes and well-being. Significant difference was found between intervention group and control group at baseline visit in pulmonary parameters, as forced vital capacity, forced expiratory volume, forced expiratory volume, transfer factor for carbon monoxide, transfer coefficient for carbon monoxide, and oxygen saturation (all p < 0.05). Our follow-up study proved that a 2-week long, patient-centered pulmonary rehabilitation program has a positive long-term effect on people with symptomatic long COVID syndrome. Our data showed significant improvement between two and three months in maximal oxygen consumption ( p < 0.05). Multidisciplinary, individualized approach may be a key element of a successful cardiopulmonary rehabilitation in long COVID conditions, which improves workload, quality of life, respiratory function, and status of patients with long COVID syndrome. LA - English DB - MTMT ER - TY - JOUR AU - Gulej, R. AU - Nyúl-Tóth, Ádám AU - Csik, B. AU - Patai, R. AU - Petersen, B. AU - Negri, S. AU - Chandragiri, S.S. AU - Shanmugarama, S. AU - Mukli, Péter AU - Yabluchanskiy, A. AU - Conley, S. AU - Huffman, D. AU - Tarantini, Stefano AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Young blood-mediated cerebromicrovascular rejuvenation through heterochronic parabiosis: enhancing blood-brain barrier integrity and capillarization in the aged mouse brain JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE PY - 2024 SN - 2509-2715 DO - 10.1007/s11357-024-01154-8 UR - https://m2.mtmt.hu/api/publication/34864803 ID - 34864803 LA - English DB - MTMT ER - TY - JOUR AU - Magyar-Sümegi, Zsófia Dina AU - Stankovics, Levente AU - Lendvai-Emmert, Dominika AU - Czigler, András AU - Hegedüs, Emőke AU - Csendes, Márk Lajos AU - Tóth, Luca AU - Ungvári, Zoltán István AU - Büki, András AU - Tóth, Péter József TI - Acute neuroendocrine changes after traumatic brain injury JF - BRAIN AND SPINE J2 - BRAIN SPINE VL - 4 PY - 2024 PG - 11 SN - 2772-5294 DO - 10.1016/j.bas.2024.102830 UR - https://m2.mtmt.hu/api/publication/34853080 ID - 34853080 N1 - * Megosztott szerzőség LA - English DB - MTMT ER - TY - JOUR AU - Kovács, Nóra AU - Bíró, Éva AU - Pikó, Péter AU - Ungvári, Zoltán István AU - Ádány, Róza TI - Age-related shifts in mental health determinants from a deprived area in the European Union: informing the national healthy aging program of Hungary JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE PY - 2024 SN - 2509-2715 DO - 10.1007/s11357-024-01182-4 UR - https://m2.mtmt.hu/api/publication/34842957 ID - 34842957 AB - Mental disorders are among the leading causes of disability worldwide, disproportionately affecting older people. This study aims to assess the mental health of elderly individuals living in a deprived region of Hungary, and to identify and estimate the weight of different determinants of mental health across different age groups. A cross-sectional study was conducted with randomly selected samples of individuals (n = 860) aged 18 years and older in Northeast Hungary. The World Health Organization Well-Being Index (WHO-5), the single-item Life Satisfaction Scale, and the 12-item General Health Questionnaire (GHQ-12) were used to measure mental health of the participants. Multiple linear regression analysis was performed to measure the association between sociodemographic and health-related variables and mental health. Overall, the mean WHO-5 score was 69.2 ± 18.1 and it showed a significant decrease by age ( p < 0.001), with the lowest score observed in aged 75 years and above ( p < 0.001). The mean life satisfaction score was 7.5 ± 1.9 and it showed a significant decreasing trend over the life course ( p < 0.001). The highest level of psychological distress as assessed by GHQ-12 was observed in the group aged 75 years or older (11.5 ± 6.0, p < 0.001). Multiple linear regression indicated that self-reported financial status, social support, sense of control over their health, activity limitation and pain intensity were the most important determinants of mental health among older adults. Interventions to improve the mental health of older adults should focus on the positive impact of social support, the reduction of financial insecurity and the use of effective pain relief medications. LA - English DB - MTMT ER - TY - JOUR AU - Pártos, Katalin AU - Major, Dávid AU - Dósa, Norbert Sándor AU - Fazekas-Pongor, Vince AU - Tabák, Ádám AU - Ungvári, Zoltán István AU - Horváth, Ildikó AU - Barta, Ildikó AU - Pozsgai, Éva AU - Bodnár, Tamás AU - Fehér, Gergely AU - Lenkey, Zsófia AU - Fekete, Mónika AU - Springó, Zsolt TI - Diagnosis rates, therapeutic characteristics, lifestyle, and cancer screening habits of patients with diabetes mellitus in a highly deprived region in Hungary: a cross-sectional analysis JF - FRONTIERS IN ENDOCRINOLOGY J2 - FRONT ENDOCRINOL VL - 15 PY - 2024 PG - 8 SN - 1664-2392 DO - 10.3389/fendo.2024.1299148 UR - https://m2.mtmt.hu/api/publication/34830215 ID - 34830215 N1 - * Megosztott szerzőség LA - English DB - MTMT ER - TY - JOUR AU - Ungvári, Zoltán István AU - Ungvári, Anna Sára AU - Bianchini, Giampaolo AU - Győrffy, Balázs TI - Prognostic significance of a signature based on senescence-related genes in colorectal cancer JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE PY - 2024 SN - 2509-2715 DO - 10.1007/s11357-024-01164-6 UR - https://m2.mtmt.hu/api/publication/34825015 ID - 34825015 N1 - Vascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Stephenson Cancer Center, University of Oklahoma, Oklahoma City, OK, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Health Promotion Sciences, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral College/Department of Public Health, Semmelweis University, Budapest, Hungary Department of Public Health, Semmelweis University, Semmelweis University, Budapest, Hungary Department of Medical Oncology, IRCCS Ospedale San Raffaele, Milan, Italy Dept. of Bioinformatics, Semmelweis University, Budapest, 1094, Hungary Dept. of Biophysics, Medical School, University of Pecs, Pecs, 7624, Hungary Cancer Biomarker Research Group, Institute of Molecular Life Sciences, HUN-REN Research Centre for Natural Sciences, Budapest, 1117, Hungary Export Date: 6 May 2024 Correspondence Address: Ungvari, A.; Department of Public Health, Hungary; email: Ungann2004@gmail.com AB - Colorectal cancer, recognized as a quintessential age-related disease, underscores the intricate interplay between aging mechanisms and disease pathogenesis. Cellular senescence, a DNA damage-induced cellular stress response, is characterized by cell cycle arrest, the expression of an inflammatory senescence-associated secretory phenotype, and alterations in extracellular matrix metabolism. It is widely recognized as a fundamental and evolutionarily conserved mechanism of aging. Guided by geroscience principles, which assert that the pathogenesis of age-related diseases involves cellular mechanisms of aging, this study delves into the role of senescence-related genes in colon cancer progression. Leveraging a gene set reflective of senescence-associated pathways, we employed uni- and multivariate Cox proportional hazards survival analysis combined with the determination of the false discovery rate to analyze correlations between gene expression and survival. The integrated database of 1130 colon cancer specimens with available relapse-free survival time and relapse event data from ten independent cohorts provided a robust platform for survival analyses. We identified senescence-related genes associated with differential expression levels linked to shorter survival. Our findings unveil a prognostic signature utilizing cellular senescence-related genes (hazard ratio: 2.73, 95% CI 2.12-3.52, p = 6.4E - 16), offering valuable insights into survival prediction in colon cancer. Multivariate analysis underscored the independence of the senescence-related signature from available epidemiological and pathological variables. This study highlights the potential of senescence-related genes as prognostic biomarkers. Overall, our results underscore the pivotal role of cellular senescence, a fundamental mechanism of aging, in colon cancer progression. LA - English DB - MTMT ER - TY - JOUR AU - Csiszar, Anna AU - Ungvári, Anna Sára AU - Patai, Roland AU - Gulej, Rafal AU - Yabluchanskiy, Andriy AU - Benyó, Zoltán AU - Kovács, Illés AU - Sótonyi, Péter AU - Kirkpartrick, Angelia C AU - Prodan, Calin I AU - Liotta, Eric M AU - Zhang, Xin A AU - Tóth, Péter József AU - Tarantini, Stefano AU - Sorond, Farzaneh A AU - Ungvári, Zoltán István TI - Atherosclerotic burden and cerebral small vessel disease : exploring the link through microvascular aging and cerebral microhemorrhages JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - in press PY - 2024 PG - 30 SN - 2509-2715 DO - 10.1007/s11357-024-01139-7 UR - https://m2.mtmt.hu/api/publication/34804161 ID - 34804161 N1 - * Megosztott szerzőség AB - 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. LA - English DB - MTMT ER - 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 N1 - Export Date: 08 May 2024 LA - English DB - MTMT ER - TY - JOUR AU - Balasubramanian, Priya AU - Kiss, Tamás AU - Gulej, Rafal AU - Nyúl-Tóth, Ádám AU - Tarantini, Stefano AU - Yabluchanskiy, Andriy AU - Ungvári, Zoltán István AU - Csiszar, Anna TI - Accelerated Aging Induced by an Unhealthy High-Fat Diet: Initial Evidence for the Role of Nrf2 Deficiency and Impaired Stress Resilience in Cellular Senescence JF - NUTRIENTS J2 - NUTRIENTS VL - 16 PY - 2024 IS - 7 PG - 18 SN - 2072-6643 DO - 10.3390/nu16070952 UR - https://m2.mtmt.hu/api/publication/34773870 ID - 34773870 AB - High-fat diets (HFDs) have pervaded modern dietary habits, characterized by their excessive saturated fat content and low nutritional value. Epidemiological studies have compellingly linked HFD consumption to obesity and the development of type 2 diabetes mellitus. Moreover, the synergistic interplay of HFD, obesity, and diabetes expedites the aging process and prematurely fosters age-related diseases. However, the underlying mechanisms driving these associations remain enigmatic. One of the most conspicuous hallmarks of aging is the accumulation of highly inflammatory senescent cells, with mounting evidence implicating increased cellular senescence in the pathogenesis of age-related diseases. Our hypothesis posits that HFD consumption amplifies senescence burden across multiple organs. To scrutinize this hypothesis, we subjected mice to a 6-month HFD regimen, assessing senescence biomarker expression in the liver, white adipose tissue, and the brain. Aging is intrinsically linked to impaired cellular stress resilience, driven by dysfunction in Nrf2-mediated cytoprotective pathways that safeguard cells against oxidative stress-induced senescence. To ascertain whether Nrf2-mediated pathways shield against senescence induction in response to HFD consumption, we explored senescence burden in a novel model of aging: Nrf2-deficient (Nrf2+/−) mice, emulating the aging phenotype. Our initial findings unveiled significant Nrf2 dysfunction in Nrf2+/− mice, mirroring aging-related alterations. HFD led to substantial obesity, hyperglycemia, and impaired insulin sensitivity in both Nrf2+/− and Nrf2+/+ mice. In control mice, HFD primarily heightened senescence burden in white adipose tissue, evidenced by increased Cdkn2a senescence biomarker expression. In Nrf2+/− mice, HFD elicited a significant surge in senescence burden across the liver, white adipose tissue, and the brain. We postulate that HFD-induced augmentation of senescence burden may be a pivotal contributor to accelerated organismal aging and the premature onset of age-related diseases. LA - English DB - MTMT ER - TY - JOUR AU - Petersen, B. AU - Negri, S. AU - Milan, M. AU - Reyff, Z. AU - Ballard, C. AU - Ihuoma, J. AU - Ungvári, Zoltán István AU - Tarantini, Stefano TI - Editorial: Endocrine regulation of aging: impacts of humoral factors and circulating mediators JF - FRONTIERS IN ENDOCRINOLOGY J2 - FRONT ENDOCRINOL VL - 15 PY - 2024 PG - 3 SN - 1664-2392 DO - 10.3389/fendo.2024.1387435 UR - https://m2.mtmt.hu/api/publication/34760823 ID - 34760823 N1 - Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Vascular Cognitive Impairment and Neurodegeneration Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Hudson College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Export Date: 6 April 2024 Correspondence Address: Tarantini, S.; Oklahoma Center for Geroscience and Healthy Brain Aging, United States; email: Stefano-tarantini@ouhsc.edu Chemicals/CAS: galectin 3, 208128-56-7; growth hormone, 36992-73-1, 37267-05-3, 66419-50-9, 9002-72-6; nicotinamide adenine dinucleotide, 53-84-9 Funding details: National Institute of General Medical Sciences, NIGMS Funding details: American Heart Association, AHA, CDA941290 Funding details: U54GM104938 Funding details: 1P20GM125528-01A1 Funding details: T32AG052363 Funding details: National Institute on Aging, NIA, K01AG073614, R21AG080775, R03AG070479 Funding text 1: The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from the National Institute on Aging (NIA R03AG070479, NIA K01AG073614 and R21AG080775), the American Heart Association (AHA CDA941290), the HEvolution Foundation, the NIA-supported Geroscience Training Program in Oklahoma (T32AG052363), the NIA-supported Oklahoma Nathan Shock Center, and the NIGMS-supported Center of Biomedical Research Excellence (CoBRE) (1P20GM125528-01A1). This research was also supported by the Oklahoma Shared Clinical and Translational Resources (U54GM104938) with an Institutional Development Award (IDeA) from NIGMS. LA - English DB - MTMT ER -