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One trend related to age effects was observed in the young age expression group (17 miRNAs expressed predominantly at 2 weeks of age, Additional file 3).
However, at 6 months of age, expression of MyHC-I and IIx decreased in transgenic mice (respectively −75%, p<0.001, −40%, p<0.05) (Figure 9A and 9C).
At 112 days of age, expression of all ATE genes showed highly significant correlations with fat mass at 112 days, albeit none were as significant as Mest (R = 0.83; Fig. 6C and D).
At E18.5 expression is seen in both the cortical and medullary tubules (Figures 1D) and by 2 weeks of age expression is still present within the kidney cortex; however, the majority of expression is localized to the collecting ducts in the papilla (Figures 1E F).
At 10 days of age, expression of human wild-type tau (tauWT) in Drosophila neurons is mildly toxic, expression of the FTDP-17 linked mutant tau (tauR406W) is moderately toxic, and expression of a phosphomimetic mutant tau in which 14 disease-associated SP/TP phosphorylation sites are mutated to glutamate (tauE14) is substantially more toxic [16] [20].
Previous clinical studies have found similar correlations between sRAGE and AGE expression levels.
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Therefore, one can think of gene-age expression as random with respect to exam timing.
MiRNAs exhibiting old-age expression included miR-21, miR-146a, and members of the miR-29 family (miRa/b/c), which exhibit low expression at young age with increasing expression at older ages (78 and 104 weeks).
The causal model analogous to that of Figure 2 but with time-varying gene expression is shown in Figure 3. Let GX kt denote a variable representing individual k's (k=1,2) gene-by-age expression at time t (here the notation GX reflects that age is an element of X).
It is feasible that upon aging expression of these markers declines on ASCs.
However, the incidence of disease decreases in the extreme elderly, when aging expression reaches its maximum, whereas progeric syndromes associate to disease.
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