@article{MTMT:34826851, title = {Treatment of type 2 diabetes mellitus in the elderly – Special considerations}, url = {https://m2.mtmt.hu/api/publication/34826851}, author = {Gadó, Klára and Tabák, Ádám and Vingender, István and Domján, Gyula and Bednárikné Dörnyei, Gabriella}, doi = {10.1556/2060.2024.00317}, journal-iso = {PHYSIOL INT}, journal = {PHYSIOLOGY INTERNATIONAL}, volume = {in press}, unique-id = {34826851}, issn = {2498-602X}, abstract = {Type 2 diabetes is a frequent chronic disease. Given its strong positive association with older age, it is a significant public health issue in elderly populations. Furthermore, the aging of the population, driven by increasing life expectancy in high and middle-income countries leads to an increasing prevalence of diabetes.}, year = {2024}, eissn = {2677-0164}, orcid-numbers = {Gadó, Klára/0000-0003-2253-5826; Tabák, Ádám/0000-0002-6234-3936; Domján, Gyula/0000-0003-0722-1538; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252} } @article{MTMT:34825015, title = {Prognostic significance of a signature based on senescence-related genes in colorectal cancer}, url = {https://m2.mtmt.hu/api/publication/34825015}, author = {Ungvári, Zoltán István and Ungvári, Anna Sára and Bianchini, Giampaolo and Győrffy, Balázs}, doi = {10.1007/s11357-024-01164-6}, journal-iso = {GEROSCIENCE}, journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)}, unique-id = {34825015}, issn = {2509-2715}, abstract = {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.}, keywords = {CANCER; Aging; colorectal cancer; senescence; Gerooncology}, year = {2024}, eissn = {2509-2723}, orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039; Győrffy, Balázs/0000-0002-5772-3766} } @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} } @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} } @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} } @article{MTMT:34797483, title = {Birthweight trends and their explanatory factors in Hungary between 1999 and 2018. an analysis of the Hungarian Tauffer registry}, url = {https://m2.mtmt.hu/api/publication/34797483}, author = {Zsirai, László and Kun, Attila and Visolyi, Gergely and Svébis, Márk Márton and Domján, Beatrix Annamária and Tabák, Ádám}, doi = {10.1186/s12978-024-01787-0}, journal-iso = {REPROD HEALTH}, journal = {REPRODUCTIVE HEALTH}, volume = {21}, unique-id = {34797483}, abstract = {The increasing birthweight trend stopped and even reversed in several high income countries in the last 20 years, however the reason for these changes is not well characterized. We aimed to describe birthweight trends of term deliveries in Hungary between 1999 and 2018 and to investigate potential maternal and foetal variables that could drive these changes.We analysed data from the Hungarian Tauffer registry, a compulsory anonymized data collection of each delivery. We included all singleton term deliveries in 1999-2018 (n = 1,591,932). We modelled birthweight trends separately in 1999-2008 and 2008-2018 in hierarchical multiple linear regression models adjusted for calendar year, newborn sex, maternal age, gestational age at delivery, and other important determinants.Median birthweights increased from 3250/3400 g (girl/boy) to 3300/3440 g from 1999 to 2008 and decreased to 3260/3400 g in 2018. When we adjusted for gestational age at delivery the increase in the first period became more pronounced (5.4 g/year). During the second period, similar adjustment substantially decreased the rate of decline from 2.5 to 1.4 g/year. Further adjustment for maternal age halved the rate of increase to 2.4 g/year in the first period. During the second period, adjustment for maternal age had little effect on the estimate.Our findings of an increasing birthweight trend (mostly related to the aging of the mothers) in 1999-2008 may forecast an increased risk of cardiometabolic diseases in offsprings born in this period. In contrast, the decreasing birthweight trends after 2008 may reflect some beneficial effects on perinatal morbidity. However, the long-term effect cannot be predicted, as the trend is mostly explained by the shorter pregnancies.}, keywords = {pregnancy; Gestational Age; parity; Maternal Age; Caesarean section; labor induction; Population-based study; birthweight; Obstetrical database; Week of delivery}, year = {2024}, eissn = {1742-4755}, orcid-numbers = {Visolyi, Gergely/0000-0003-3677-7682; Svébis, Márk Márton/0000-0002-6624-9621; Tabák, Ádám/0000-0002-6234-3936} } @article{MTMT:34777041, title = {Dohányzó várandósok elsődleges védőnői állapotfelmérése az alapellátásban}, url = {https://m2.mtmt.hu/api/publication/34777041}, author = {Rákóczi, Ildikó and Balázs, Péter and Foley, Kristie L.}, doi = {10.1556/650.2024.33014}, journal-iso = {ORV HETIL}, journal = {ORVOSI HETILAP}, volume = {165}, unique-id = {34777041}, issn = {0030-6002}, abstract = {Bevezetés: A várandósok dohányzása számos szülészeti és neonatológiai szövődményt okozhat. Megelőzésükre szervezetileg kiváló lehetőség a gondozásba vételkor a dohányzói status védőnői felmérése, majd a háziorvosokkal együtt a várandósok támogatása a dohányzás szünetelése vagy a leszokás érdekében. Célkitűzés: Egy mintaszerű rendszer felépítésére Nyíregyházán modellkísérletet végeztünk a városi védőnői hálózatban 2019. október 1. és 2021. március 31. között, gondozásra jelentkezett várandósok körében. Módszer: Papíralapú kérdőíveink kitöltését a védőnők végezték a gondozásba vételkor a várandósok válaszai alapján. A legfőbb biometriai, szociodemográfiai és családtervezési adatokon (9 kérdés) túl a dohányzási (cigarettázási) szokásokat, a környezeti dohányfüstártalmat és a dohányzás ártalmasságának ismeretét vizsgáltuk (9 kérdés). A statisztikai vizsgálatot frekvencia- és kereszttáblás elemzéssel végeztük. Szignifikánsnak fogadtuk el az eredményeket p<0,05 értékkel. Eredmények: A gondozásba vett összes várandós (n = 1761) közül 1548 (87,9%) válaszolt a kérdéseinkre. Mintánk átlagéletkora 30,2 év (min./max.: 15/48) volt, gondozásba vételük átlagosan a várandósság 10,8. hetében (min./max.: 6/34) történt. Jelentős volt a magasabb fokú iskolai végzettséggel (középfokú 46,0%, felsőfokú 42,8%) rendelkezők aránya. A roma nemzetiség aránya 4,2% volt. Tervezett volt a várandósság 88,5%-ban. Soha nem dohányzott 46,5%. Dohányzói anamnézise volt 53,5%-nak. A teljes mintából 10,1% folytatta a dohányzást, de 42,5% korábbi dohányos azt állította, hogy aktuálisan nem cigarettázik. A férjek/élettársak (n = 1493) részéről 30,3%-ban fordult elő környezeti dohányfüstártalom. Minden várandós (98,9%) tisztában volt a dohányzás magzatkárosító hatásával. Következtetés: Nagyvárosi környezetben a magasabb szintű iskolai végzettség hozzájárult a dohányzás magzatkárosító hatásának ismeretéhez. A várandósság alatt tovább folytatott dohányzásban a romák szignifikánsan hátrányosabb helyzetben voltak a nem romákkal szemben. Másodlagos dohányfüstártalom szempontjából nagyon kedvezőtlen volt a férj/élettárs dohányzásának csaknem egyharmados aránya. Az alapellátás a legegyszerűbben a védőnők révén érheti el a dohányzás által különösen veszélyeztetett populációt. Részükre a bemutatott módszerrel a háziorvos és a védőnő az adatok alapján célzottan végezheti a dohányzással kapcsolatban az alapellátás kompetenciájába tartozó szünetelés/leszokás támogatást. Orv Hetil. 2024; 165(14): 545–552.}, year = {2024}, eissn = {1788-6120}, pages = {545-552}, orcid-numbers = {Balázs, Péter/0000-0001-7351-4828} } @article{MTMT:34771724, title = {Impact of visceral adipose tissue on longevity and metabolic health: a comparative study of gene expression in perirenal and epididymal fat of Ames dwarf mice}, url = {https://m2.mtmt.hu/api/publication/34771724}, author = {Zaczek, A. and Lewiński, A. and Karbownik-Lewińska, M. and Lehoczki, Andrea Marianna and Gesing, A.}, doi = {10.1007/s11357-024-01131-1}, journal-iso = {GEROSCIENCE}, journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)}, volume = {in press}, unique-id = {34771724}, issn = {2509-2715}, abstract = {Emerging research underscores the pivotal role of adipose tissue in regulating systemic aging processes, particularly when viewed through the lens of the endocrine hypotheses of aging. This study delves into the unique adipose characteristics in an important animal model of aging — the long-lived Ames dwarf (df/df) mice. Characterized by a Prop1df gene mutation, these mice exhibit a deficiency in growth hormone (GH), prolactin, and TSH, alongside extremely low circulating IGF-1 levels. Intriguingly, while surgical removal of visceral fat (VFR) enhances insulin sensitivity in normal mice, it paradoxically increases insulin resistance in Ames dwarfs. This suggests an altered profile of factors produced in visceral fat in the absence of GH, indicating a unique interplay between adipose tissue function and hormonal influences in these models. Our aim was to analyze the gene expression related to lipid and glucose metabolism, insulin pathways, inflammation, thermoregulation, mitochondrial biogenesis, and epigenetic regulation in the visceral (perirenal and epididymal) adipose tissue of Ames dwarf and normal mice. Our findings reveal an upregulation in the expression of key genes such as Lpl, Adrβ3, Rstn, Foxo1, Foxo3a, Irs1, Cfd, Aldh2, Il6, Tnfα, Pgc1α, Ucp2, and Ezh2 in perirenal and Akt1, Foxo3a, PI3k, Ir, Acly, Il6, Ring1a, and Ring 1b in epididymal fat in df/df mice. These results suggest that the longevity phenotype in Ames dwarfs, which is determined by peripubertal GH/IGF-1 levels, may also involve epigenetic reprogramming of adipose tissue influenced by hormonal changes. The increased expression of genes involved in metabolic regulation, tumor suppression, mitochondrial biogenesis, and insulin pathways in Ames dwarf mice highlights potentially beneficial aspects of this model, opening new avenues for understanding the molecular underpinnings of longevity and aging. © The Author(s), under exclusive licence to American Aging Association 2024.}, keywords = {Inflammation; Aging; MITOCHONDRIAL BIOGENESIS; AMES DWARF MICE; Insulin pathway; Lipid and glucose metabolism}, year = {2024}, eissn = {2509-2723} } @article{MTMT:34771485, title = {Combining detrended cross-correlation analysis with Riemannian geometry-based classification for improved brain-computer interface performance}, url = {https://m2.mtmt.hu/api/publication/34771485}, author = {Rácz, Frigyes Sámuel and Kumar, S. and Káposzta, Zalán and Alawieh, H. and Liu, D.H. and Liu, R. and Czoch, Ákos and Mukli, Péter and Millán, J.D.R.}, doi = {10.3389/fnins.2024.1271831}, journal-iso = {FRONT NEUROSCI-SWITZ}, journal = {FRONTIERS IN NEUROSCIENCE}, volume = {18}, unique-id = {34771485}, issn = {1662-4548}, abstract = {Riemannian geometry-based classification (RGBC) gained popularity in the field of brain-computer interfaces (BCIs) lately, due to its ability to deal with non-stationarities arising in electroencephalography (EEG) data. Domain adaptation, however, is most often performed on sample covariance matrices (SCMs) obtained from EEG data, and thus might not fully account for components affecting covariance estimation itself, such as regional trends. Detrended cross-correlation analysis (DCCA) can be utilized to estimate the covariance structure of such signals, yet it is computationally expensive in its original form. A recently proposed online implementation of DCCA, however, allows for its fast computation and thus makes it possible to employ DCCA in real-time applications. In this study we propose to replace the SCM with the DCCA matrix as input to RGBC and assess its effect on offline and online BCI performance. First we evaluated the proposed decoding pipeline offline on previously recorded EEG data from 18 individuals performing left and right hand motor imagery (MI), and benchmarked it against vanilla RGBC and popular MI-detection approaches. Subsequently, we recruited eight participants (with previous BCI experience) who operated an MI-based BCI (MI-BCI) online using the DCCA-enhanced Riemannian decoder. Finally, we tested the proposed method on a public, multi-class MI-BCI dataset. During offline evaluations the DCCA-based decoder consistently and significantly outperformed the other approaches. Online evaluation confirmed that the DCCA matrix could be computed in real-time even for 22-channel EEG, as well as subjects could control the MI-BCI with high command delivery (normalized Cohen's κ: 0.7409 ± 0.1515) and sample-wise MI detection (normalized Cohen's κ: 0.5200 ± 0.1610). Post-hoc analysis indicated characteristic connectivity patterns under both MI conditions, with stronger connectivity in the hemisphere contralateral to the MI task. Additionally, fractal scaling exponent of neural activity was found increased in the contralateral compared to the ipsilateral motor cortices (C4 and C3 for left and right MI, respectively) in both classes. Combining DCCA with Riemannian geometry-based decoding yields a robust and effective decoder, that not only improves upon the SCM-based approach but can also provide relevant information on the neurophysiological processes behind MI. Copyright © 2024 Racz, Kumar, Kaposzta, Alawieh, Liu, Liu, Czoch, Mukli and Millán.}, keywords = {DETRENDED FLUCTUATION ANALYSIS; ONLINE; Brain-computer Interface; Detrended Cross-Correlation Analysis; motor imagery; Fractal connectivity; Reimannian geometry}, year = {2024}, eissn = {1662-453X}, orcid-numbers = {Rácz, Frigyes Sámuel/0000-0001-9077-498X; Mukli, Péter/0000-0003-4355-8103} } @article{MTMT:34760823, title = {Editorial: Endocrine regulation of aging: impacts of humoral factors and circulating mediators}, url = {https://m2.mtmt.hu/api/publication/34760823}, author = {Petersen, B. and Negri, S. and Milan, M. and Reyff, Z. and Ballard, C. and Ihuoma, J. and Ungvári, Zoltán István and Tarantini, Stefano}, doi = {10.3389/fendo.2024.1387435}, journal-iso = {FRONT ENDOCRINOL}, journal = {FRONTIERS IN ENDOCRINOLOGY}, volume = {15}, unique-id = {34760823}, issn = {1664-2392}, year = {2024}, eissn = {1664-2392}, orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039; Tarantini, Stefano/0000-0001-5627-1430} }