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Blood Diseases Department of Clinical... 1 Department of Biomedical Sciences Uni... 1 Department of Regenerative Medicine R... 1 Faculty of Veterinary Medicine Univer... 1 Health and Biological Sciences Depart... 1 National Laboratory of Molecular Biol... 1 Research Department Rinaldi Fontani F... 1
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Blood Diseases Department of Clinical... 1 Department of Biomedical Sciences Uni... 1 Department of Regenerative Medicine R... 1 Faculty of Veterinary Medicine Univer... 1 Health and Biological Sciences Depart... 1 National Laboratory of Molecular Biol... 1 Research Department Rinaldi Fontani F... 1
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Free Medical Journals od 1998
PubMed Central od 2020
ProQuest Central od 2005-01-01
Medline Complete (EBSCOhost) od 2006-01-01
Nursing & Allied Health Database (ProQuest) od 2005-01-01
Health & Medicine (ProQuest) od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources od 1998
PubMed
35899943
DOI
10.33549/physiolres.934903
Knihovny.cz E-zdroje
About 30 percent of patients diagnosed with myelodysplastic syndromes (MDS) progress to acute myeloid leukemia (AML). The senescence of bone marrow?derived mesenchymal stem cells (BMSCs) seems to be one of the determining factors in inducing this drift. Research is continuously looking for new methodologies and technologies that can use bioelectric signals to act on senescence and cell differentiation towards the phenotype of interest. The Radio Electric Asymmetric Conveyer (REAC) technology, aimed at reorganizing the endogenous bioelectric activity, has already shown to be able to determine direct cell reprogramming effects and counteract the senescence mechanisms in stem cells. Aim of the present study was to prove if the anti-senescence results previously obtained in different kind of stem cells with the REAC Tissue optimization - regenerative (TO-RGN) treatment, could also be observed in BMSCs, evaluating cell viability, telomerase activity, p19ARF, P21, P53, and hTERT gene expression. The results show that the REAC TO-RGN treatment may be a useful tool to counteract the BMSCs senescence which can be the basis of AML drift. Nevertheless, further clinical studies on humans are needed to confirm this hypothesis.
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