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These data suggest that aPKCλ-defective cells show defects in the development of tight junctions.
Surprisingly, these mice did not exhibit any apparent morphological defects in the development of normal retinal vasculature.
As such, impaired skeletal muscle insulin action and glucose utilization are the primary defects in the development of type 2 diabetes (DeFronzo and Tripathy, 2009).
APP−/−APLP2−/− animals show dramatic defects in the development of NMJ [29], [31].
Interestingly, we found no major defects in the development or function of the central nervous system.
This was due to profound defects in the development of antiviral effector CD4 and CD8 T cell response in old mice [9].
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AhR −/− mice have a defect in the development of LTi cells and thus lack tertiary lymphoid structure cryptopatches (CPs) and isolated lymphoid follicles (ILFs) in the gut (Kiss et al., 2011).
Thus, a defect in the development of the ventricle wall of the heart appears to be the most likely cause of death in GPR126 mutants.
It has previously been shown that loss of a single Vegfa allele in mice can result in embryonic lethality by embryonic day 11.5 due to a defect in the development of labyrinthine trophoblast cells [24].
It has been reported that the embryonic lethality of Ire1α−/− mice is due to the defect in the development of the labyrinthine trophoblast cells which are critical for integration and exchange between fetal and maternal blood vessels in the placenta [23].
Moreover, phenotypic analysis of the DN γδ thymocytes and mature DN γδ T cells from WT, Lck+/− and Fyn+/− mice revealed no appreciable differences in Vγ usage, TCRγδ surface levels and cell surface phenotype (data not shown), indicating that reducing the expression levels of Lck or Fyn resulted in no apparent defect in the development of polyclonal γδ T cells.
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