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To better understand these environmental-induced cell changes, we have modeled the germ layer formation process by culturing human embryonic stem cells (hESCs) on three dimensional (3D) scaffolds with stiffness engineered to model that found in specific germ layers.
However, as these pathways regulate germ layer formation and patterning, their specific roles in cardiac induction have been difficult to define.
Endoderm and mesoderm germ layer formation in vertebrate embryos requires the activity of the conserved TGFβ/Nodal signaling pathway [1], [2], [3], [4], [5], [6].
Studies of morphogen gradients have shown that Nodal is a key TGFβ morphogen in vertebrate development responsible for gastrulation, germ layer formation and patterning, i.e. shaping the embryo by specifying the axes of the body plan [10].
In the following experiments our objective was to modulate the signalling pathways that may be involved in the interpretation of the signal while avoiding interference with the production of the signal, as this would likely also affect normal germ layer formation and patterning of the embryonic axes with the potential to influence cardiogenesis indirectly.
Based on Xenopus study, we propose a model for the germ layer formation.
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Actually, it is a challenge to address this issue because the 'non-fully-pluripotent' iPSCs are a wide variety of iPSCs including iPSCs only capable of differentiation into the three germ layers, formation of teratomas, embryoid body, chimeric mice or dead all-iPSC pups, respectively.
From 1819 to 1834 Baer devoted most of his time to embryology, extending Pander's concept of germ-layer formation to all vertebrates.
This trimester is the period of greatest susceptibility to teratogens, since it is when germ-layer formation and organogenesis occur, defined as up to and including 12 gestational weeks.
The strategy of coupling changes in cell adhesion to transcriptional control of cell fate specification is used several times during development as a way of coordinating tissue morphogenesis (Owens et al., 2000; Martínez-Estrada et al., 2010; Watt and Fujiwara, 2011), and it will be interesting to investigate the implications of our findings for germ-layer formation in the early embryo.
In direct contrast, testes transplanted with undifferentiated H9 (Fig. 4Av) and H1 (Fig. 4Aiii) hESCs, developed enlarged tissues indicative of tumors similar to OSKM cells (Fig. 4Aii) and in addition formed teratoma-like structures (in H9 cells only, Fig. 4Avi) indicative of multiple germ layer tissue formation (see also Supplementary Material, Table S3).
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