Previous results in the Gcdh−/− mice fed with a high lysine diet showed BBB defects evidenced by a progressive disappearance of occludin with no changes in ZO-1 expression [ 13].
Moreover, it produced an epidermal differentiation defect evidenced by the lack of loricrin and filaggrin expression in the epidermis.
This was in spite of proper representation of BM precursors, and rather reflected a peripheral defect evidenced by the disrupted architecture of the spleen.
No HAC or PMMA augmented defects showed evidence of subchondral fracture.
The DLE contribution is conventionally attributed to oxygen vacancies and other bulk lattice defects, despite evidence pointing to surface defects for nanostructures [17, 18].
In contrast, embryos homozygous for a mutation in K-ras die between 12 and 14 days of gestation, with foetal liver defects and evidence of anaemia [8].
Furthermore those species with UGT1A6 defects showed evidence for reduced amino acid constraint (increased dN/dS ratios approaching the neutral selection value of 1.0) as compared with species with intact UGT1A6.
Although immunofluorescence analysis indicated Shg expression was maintained overall in Dcas null embryos, the 10% of embryos with GBR/DC defects had evidence of mislocalized Shg, with greater accumulation in a disorganized pool of Shg at the lateral and basal cell surface.
For birth defects, the evidence base so far is insufficient to draw conclusions.
Cartilage defects are evidence of early cartilage pathology, independent of cartilage volume [ 21].
For other effects such as changes in the immune system and birth defects, the evidence is limited.
