Evidence map›Paper›PMID 35899943›Full record

ArticlePhysiological research2022

Antisenescence effect of REAC biomodulation to counteract the evolution of myelodysplastic syndrome.

M Maioli, S Rinaldi, S Cruciani, A Necas, V Fontani, G Corda, S Santaniello, A Rinaldi, Arp Barcessat, A Necasova and 4 more

Open access · goldAbstract read
In one paragraph

Article in Physiological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 3 countries.

M MaioliDepartment of Biomedical Sciences, University of Sassari, Sassari, Italy. mmaioli@uniss.it.
S Rinaldi
S Cruciani
A Necas
V Fontani
G Corda
S Santaniello
A Rinaldi
Arp Barcessat
A Necasova
A Castagna
Z Filipejova
C Ventura
C Fozza
University of Sassari · ITDeutsches Historisches Institut Rom · ITUniversity of Veterinary Sciences Brno · CZIstituto Nazionale Biostrutture e Biosistemi · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Leukemia, Myeloid, AcuteMyelodysplastic SyndromesTelomeraseCell DifferentiationHumansTumor Suppressor Protein p53TelomeraseTumor Suppressor Protein p53

Identifiers

PMID35899943
PMCPMC9616590
OpenAlexW4288751540

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.