Analysis of Sall2-deficient mouse embryos revealed delayed apposition of the optic fissure margins and the persistence of an anterior retinal coloboma phenotype after birth.
Finally, the analysis of subretinal vascularization revealed delayed angiogenesis in Bst+/– mice associated with delayed hyaloid regression.
Determination of cell proliferation, by Ki67-positive cell count in liver sections, revealed delayed progression in the cell cycle in TRα1/TRβ KO and MMI-treated mice (Fig. 2B), while flow cytometry of disaggregated liver cells showed no significant differences in the ploidy distribution among the animal groups (Fig. 2C).
ITGB1 is not essential for fertilization in mice based on studies of an oocyte-specific Itgb1 conditional knockout [21], although Itgb1-deficient eggs do have subtle defects, as recent studies have revealed delayed sperm binding to Itgb1-deficient eggs [22], in agreement with observations of reduced sperm binding to eggs treated with anti-ITGB1 antibodies [10], [14], [19], [23].
As shown in Figure 4, Y1 receptor KO mice revealed significantly delayed extinction of conditioned fear.
Ultrastructural analysis of the corneodesmosomes in control and K5cre-CMVcaNrf2 mice revealed a delay in corneodesmosome degradation in transgenic mice (Fig 6D).
Lack of P2Y12 in knockout mice revealed a significant delay but no complete abolishment of microglial chemotaxis [60].
An in vivo study on the anticancer activity of MOE on B16 F10 melanoma tumors in mice, revealed that treatment at 500 mg/kg-bw could delay tumor growth and increase lifespan [ 20].
Whereas IFN-γ has previously been shown to exert antifibrotic effects in man and mice by abrogating TGF-β signalling [ 31, 32], inducing an acute liver damage in IFN-γ knockout mice revealed that the degree of damage was reduced and delayed when compared to control mice.
Beginning in early 1990 McDonnell Douglas and General Dynamics revealed delays and projected cost increases.
