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The expression of the cell cycle marker, Ki67, was also assessed during rat heart development and was shown to be absent from the adult heart.
(K ) RT-PCR analysis of Pcnt B and S isoform expression during rat heart development in vivo.
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This issue has been highlighted by Awad et al. [ 41] who investigated the vulnerability of the intact rat heart during different stages of development (4, 7, 14, and 21 days, and adult).
Following normal development of the rat heart, the FD of nuclear chromatin of cardiomyocytes diminished significantly (r = -0.603; p = 0.001; Spearman rank order correlation) with increasing age [133].
Varying doses of each were given in drinking water to pregnant rats during the period of fetal heart development.
Based on our hypothesis that immaturity and stagnation of intracavitary flow would play a key role in the development of EFE, we reported our results on EFE development in a heterotopically transplanted neonatal rat heart model, where the LV had no intracavitary flow (i.e., preload) [ 21].
Therefore, functional α2A and α2B subtypes are present in the fetal rat heart where they may have a role in cardiac development.
The first experiment determined the effect of early development on the sphingomyelin (SM) composition of rat heart and liver tissues.
For example, about 30% of the genes that carry the GO term "heart development (GO 0007507)" were covered by our method (34% for mouse, 28% for rat, 37% for human, and 37% for chicken).
To identify genes involved in regulating vertebrate heart development, gene expression changes were analyzed in cardiomyocytes that were isolated from various stages of fetal and postnatal rat hearts (Nechiporuk et al., 2001).
The researchers removed all the cells from a dead rat heart, leaving the valves and outer structure as scaffolding for new heart cells injected from newborn rats.
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