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The studies by Kyng and Bohr (2005) and Csoka and colleagues (2004b) point to a shared mechanism of aging acceleration in PSs ie, misregulated transcription.
Our results indicated that having an aging acceleration rate that is one standard deviation above the mean (standardized IEA A = 1) is associated with as a high as a 2.5-fold increase in the risk of developing lung cancer.
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The long-term aging shift function is determined as a function of aging time, acceleration factor, activation energy, and aging temperature.
DNA methylation has an inheritable effect with age acceleration and is close to zero at the embryonic stage of an individual (Guo et al., 2014; Horvath, 2013).
In 486 monozygotic twins, we investigated the association of DNAmAge, difference between DNAmAge and chronological age and age acceleration with cognition.
The age acceleration starts with a high degree of correlation in genomic DNA methylation marks in a broad range of human tissues and cells and is influenced by gender, genetic makeup (Hannum et al., 2012), racial (Kader & Ghai, 2016; Park et al., 2016), clinical as well as lifestyle of an individual (Weidner et al., 2014).
Data S6 Results for Supplementary data file for relating CpGs with age acceleration and DS status.
To formally measure age acceleration effects, we defined age acceleration as the residual resulting from a linear model that regressed DNAm age against chronological age in non-cerebellar brain sample.
Fig. s4 Blood cell types versus age acceleration in dataset 1. Fig. s5 Blood cell types versus age acceleration in dataset 3. Fig. s6 Results for alternative epigenetic biomarkers of aging.
Fig. s7 Preservation of marginal associations with age and age acceleration Fig. s8 Preservation of associations with DS status.
Thus, a tissue sample that exhibits negative age acceleration appears to be younger than expected based simply on chronological age.
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