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Our data suggest that the alveolar phenotype of Cby−/− mice results, at least in part, from reduced proliferation and altered differentiation of epithelial cells rather than septation defects (Figures 5 and 6).
The two LmnaE82K transgenic mice lines exhibited chamber dilation, increased heart weights, increased fibrosis, upregulation of hypertrophic maker expression, nuclear structure defects and conduction defects (Figures 1, 2, 3, Tables 1, 2), which was similar with the phenotypes of the patients carrying the LMNA E82K mutation.
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Adding another 250 temperature cycles did not cause any additional defects (Figure 8c).
Retroillumination images at presentation and 2 weeks later showed stable iris transillumination defects (Figure 1E,F,G,H), suggesting an acute, self-limited injury.
However, the carbon walls of our CNFs contain defects (Figure 2b), and hence, they exhibit a disordered structure similar to disordered graphite layers, higher membered carbon rings (e.g. seven- and eight-membered rings), and disjointedness in graphite layers.
When Mad was maternally depleted, embryos displayed segmental patterning defects (Figure 6).
We also found many lines with specific CNS axon defects (Figure 2).
Results showed a significant increase in new bone area among hASC treated defects (Figure 4B).
In our study, single depletion of HP1gamma was sufficient to cause mitotic defects (Figure 6).
yata mutants also displayed various eye defects, including irregular arrangement of ommatidia, black discoloration, and lens defects (Figure 3D 3I).
The embryos that deposited cuticle exhibited a wide range of both anteroposterior and dorsoventral patterning defects (Figure 2B).
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