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These molecules exhibited an extraordinary high in vitro potency in the chick heart invasion assay, being active up to 10 nmol L−1, a concentration level a 100-fold lower than the lowest effective doses that have been reported for natural analogues.
CT26 cells were not observed in the chick heart under any condition (results not shown).
Such a role for fluid dynamics has been demonstrated in early chick heart development [25].
Still, there is no direct evidence to demonstrate that cNkx2.8 can compensate for cNkx2.5 loss of function in early development of chick heart.
Expression studies localised eMYH in the developing chick heart.
We conclude that OLFM1 is present and necessary during EMT in the embryonic chick heart.
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We also found reduced titin N2BA-to-N2B expression ratios in hypoxic chick hearts.
Levels of the sarcomeric proteins titin (Figure 2D E) and myosin heavy chain (MHC, Table 1) were lowered in hypoxic embryonic chick hearts.
Lowering VEGF levels in hypoxic embryonic chick hearts by systemic administration of sFlt-1 yielded an almost complete normalization of the phenotype.
Embryonic chick hearts have been used as primary cell lines for the study of cardiovascular functions and maturation.
Using an in vitro invasion assay, an extracellular matrix protein, Olfactomedin-1 (OLFM1), was found to increase mesenchymal cell numbers in AV canals from embryonic chick hearts.
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