PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7645
Browse
Search Results
Article Meal Timing Trajectories in Older Adults and Their Associations With Morbidity, Genetic Profiles, and Mortality(Springernature, 2025) Dashti, Hassan S.; Liu, Chloe; Deng, Hao; Sharma, Anushka; Payton, Antony; Maharani, Asri; Didikoglu, AltugBackgroundOlder adults are vulnerable to mistimed food intake due to health and environmental changes; characterizing meal timing may inform strategies to promote healthy aging. We investigated longitudinal trajectories of self-reported meal timing in older adults and their associations with morbidity, genetic profiles, and all-cause mortality.MethodsWe analyzed data from 2945 community-dwelling older adults from the University of Manchester Longitudinal Study of Cognition in Normal Healthy Old Age, with up to five repeated assessments of meal timing and health behaviors conducted between 1983 and 2017. Linear mixed-effects models, latent class analysis, and Cox regression were used to examine relationships between meal timing with illness and behavioral factors, genetic scores for chronotype and obesity, and mortality.ResultsHere we show older age is associated with later breakfast and dinner times, a later eating midpoint, and a shorter daily eating window. Physical and psychological illnesses, including fatigue, oral health problems, depression, anxiety, and multimorbidity, are primarily associated with later breakfast. Genetic profiles related to an evening chronotype, but not obesity, are linked to later meals. Later breakfast timing is also associated with increased mortality. Latent class analysis of meal timing trajectories identify early and late eating groups, with 10-year survival rates of 86.7% in the late eating group compared to 89.5% in the early eating group.ConclusionsMeal timing, particularly later breakfast, shifts with age and may reflect broader health changes in older adults, with implications for morbidity and longevity.Article A Comprehensive MicroRNA-Seq Transcriptomic Analysis of Tay-Sachs Disease Mice Revealed Distinct MiRNA Profiles in Neuroglial Cells(Springernature, 2025) Kaya, Beyza; Orhan, Mehmet Emin; Yanbul, Selman; Demirci, Muserref Duygu Sacar; Demir, Secil Akyildiz; Seyrantepe, VolkanTay-Sachs disease (TSD) is a rare lysosomal storage disorder marked by the progressive buildup of GM2 in the central nervous system (CNS). This condition arises from mutations in the HEXA gene, which encodes the alpha subunit of the enzyme beta-hexosaminidase A. A newly developed mouse model for early-onset TSD (Hexa-/-Neu3-/-) exhibited signs of neurodegeneration and neuroinflammation, evidenced by elevated levels of pro-inflammatory cytokines and chemokines, as well as significant astrogliosis and microgliosis. Identifying disease-specific microRNAs (miRNAs) may aid the development of targeted therapies. Although previous small-scale studies have investigated miRNA expression in some regions of GM2 gangliosidosis mouse models, thorough profiling of miRNAs in this innovative TSD model remains to be done. In this study, we employed next-generation sequencing to analyze the complete miRNA profile of neuroglial cells from Hexa-/-Neu3-/- mice. By comparing KEGG and Reactome pathways associated with neurodegeneration, neuroinflammation, and sphingolipid metabolism in Hexa-/-Neu3-/- neuroglial cells, we discovered new microRNAs and their targets related to the pathophysiology of GM2 gangliosidosis. For the first time, our findings showed that miR-708-5p, miR-672-5p, miR-204-5p, miR-335-5p, and miR-296-3p were upregulated, while miR-10 b-5p, miR-615-3p, miR-196a-5p, miR-214-5p, and miR-199a-5p were downregulated in Hexa-/-Neu3-/- neuroglial cells in comparison to age-matched wild-type (WT). These specific changes in miRNA expression deepen our understanding of the disease's neuropathological characteristics in Hexa-/-Neu3-/- mice. Our study suggests that miRNA-based therapeutic strategies may improve clinical outcomes for TSD patients.Article Citation - WoS: 1Citation - Scopus: 1The Role of Trna Fragments on Neurogenesis Alteration by H2o2-Induced Oxidative Stress(Springernature, 2025) Karacicek, Bilge; Katkat, Esra; Binokay, Leman; Ozhan, Gunes; Karakulah, Goekhan; Genc, SerminTransfer RNAs (tRNAs) are small non-coding RNA molecules transcribed from tRNA genes. tRNAs cleaved into a diverse population tRNA fragments (tRFs) ranging in length from 18 to 40 nucleotides, they interact with RNA binding proteins and influence the stability and translation. Stress is one of the reasons for tRFs cleavage. In our study, we modeled oxidative stress conditions with hydrogen peroxide (H2O2) exposure and dealt with one of the frequently expressed tRF in the hippocampus region of the brain, which is tRF-Glu-CTC. For this purpose, neural stem cells (NSCs) were exposed to H2O2, and tRF-Glu-CTC levels were increased in various H(2)O(2 )concentrations. A decrease was seen in microtubule-associated protein 2 (MAP2) marker expression. To understand the H(2)O(2)oxidative stress condition on the expression of tRNA fragments, 72 hpf zebrafish embryos exposed to different H(2)O(2 )concentrations, an increase in the level of tRF-Glu-CTC was observed in all concentrations of H(2)O(2 )compared to control. Subsequently, neurogenesis markers were figured out via Calb2a (calbindin 2a) in situ hybridization (ISH) and HuC/D immunofluorescence staining (IF) staining experiments. Under H(2)O(2 )exposure, a decline was observed in Calb2a and HuC/D markers. To understand the inhibitory role of tRF-Glu-CTC on neurogenesis, NSCs were transfected via tRF-Glu-CTC inhibitor, and neurogenesis markers (ss III-tubulin, MAP2, and GFAP) were determined with qRT-PCR and IF staining. tRF-Glu-CTC inhibitor reversed the diminished neuronal markers expression under the exposure of H2O2. Gene Ontology (GO) enrichment analysis showed us that targets of tRF-Glu-CTC are generally related to neuronal function and synaptic processes.Article Citation - WoS: 1Tcgex: a Powerful Visual Interface for Exploring and Analyzing Cancer Gene Expression Data(Springernature, 2025) Kus, M. Emre; Sahin, Cagatay; Kilic, Emre; Askin, Arda; Ozgur, M. Mert; Karahanogullari, Gokhan; Ekiz, H. AtakanAnalyzing gene expression data from the Cancer Genome Atlas (TCGA) and similar repositories often requires advanced coding skills, creating a barrier for many researchers. To address this challenge, we developed The Cancer Genome Explorer (TCGEx), a user-friendly, web-based platform for conducting sophisticated analyses such as survival modeling, gene set enrichment analysis, unsupervised clustering, and linear regression-based machine learning. TCGEx provides access to preprocessed TCGA data and immune checkpoint inhibition studies while allowing integration of user-uploaded data sets. Using TCGEx, we explore molecular subsets of human melanoma and identify microRNAs associated with intratumoral immunity. These findings are validated with independent clinical trial data on immune checkpoint inhibitors for melanoma and other cancers. In addition, we identify cytokine genes that can be used to predict treatment responses to various immune checkpoint inhibitors prior to treatment. Built on the R/Shiny framework, TCGEx offers customizable features to adapt analyses for diverse research contexts and generate publication-ready visualizations. TCGEx is freely available at https://tcgex.iyte.edu.tr, providing an accessible tool to extract insights from cancer transcriptomics data.