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Moreover, it also implies that cardiac progenitors can be autonomously re- and even pre-programmed in the early embryo to protect against pathological heart phenotypes later in life.
These results indicate that aberrant phosphorylation (lower or higher) of Hand1 caused pathological heart remodeling.
Hand1 was also found to play a role in pathological heart remodeling in human and rodent models [16], [17].
Such studies have contributed to developing many models that explain some functional aspects of normal and pathological heart [2].
In the future, it will be worthwhile to search for Hand1 mutations in patients with pathological heart remodeling, such as hypertrophic and dilated cardiomyopathy (HCM and DCM).
Hand1-AA and –DD TG mice showed increased expression of Bnp, βMhc and Anf at 1 month indicating pathological heart remodeling (Figure 1G).
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It is arguable that the differences in cardiac primitive cell biological properties observed in the presence of different culture substrates (ECM deposited by normal and pathological heart-derived fibroblasts) reflect the changes in fibroblast synthesis and secretory activity, and thus in biomatrix composition.
Here, seven proteins were differentially expressed in pathological hearts where myosin light chain 2 and 3, desmin, prohibitin, heart fatty acid binding protein, and ATP-synthase 5 β were downregulated, while heat shock proteins 60, 70, and D1 were upregulated.
ECM effects on cardiac primitive cell properties and their role in normal and pathological human heart are presented by C. Castaldo and collaborators.
This evidence might support the hypothesis that both the management of suspicious or pathological fetal heart rate tracings and of abnormal labour differed among centers.
Although the research by Fulton and Baroldi showed ample evidence of their existence in the normal and pathological human heart, nothing much was known about the mechanism of their structural enlargement.
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