ArticleJournal of community genetics2011
Hypothesis: epigenetic effects will require a review of the genetics of child development.
Article in Journal of community genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Ethanol induced acetylation of histone at G9a exon1 and G9a-mediated histone H3 dimethylation leads to neurodegeneration in neonatal mice.Neuroscience · 2014Article
- G9a-mediated histone methylation regulates ethanol-induced neurodegeneration in the neonatal mouse brain.Neurobiology of disease · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The worldwide prevalence of developmental disorders in children including birth defects, mental dysfunctions, as well as early-life abnormalities leading to the predisposition for adult diseases is one of the major unsolved problems in medicine and societies. Child development is influenced by both genes and the environment; however, the role of the environment is more emphatic, since the genome is most vulnerable to environmental factors during early development due to the high cellular differentiation rate. This inherent characteristic of child development lays the stress on a probabilistic rather than a deterministic view with regard to the manifestation of developmental disorders. Therefore, the analysis of gene-environment interactions in child development, beyond providing information about the developmental disorders of children, has an additional value that contributes to the knowledge on epigenetics in general and the interface between the genome and the environment playing a significant part in causing a wide range of diseases, in particular. The present study, rather than attempting to give a complete overview on epigenetics, is intended to illustrate that the issue of child development is an attractive target to extend the scope of genetics both in health and disease. Since the results might be extrapolated to the understanding of the pathomechanism of many age-dependent multifactorial diseases, the importance of studying gene-environment interaction in child development also lies in identifying new and potentially modifiable risk factors for diseases that are, therefore, of public health significance.
Identifiers
What OpenQuestion holds
Registered trials
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.