We propose that in the mammary gland, as has been reported in other developmental systems, Notch activation acts as a regulator of asymmetric cell-fate decisions.
This adolescent decrease in DMPFC activity during social cognition tasks seems to be a robust finding in the literature: an age-associated decrease in activity within DMPFC during adolescence has been reported in nine developmental fMRI studies that have used a variety of mentalizing tasks (for meta-analyses see Blakemore, 2008, 2010).
However, similar correlations have been reported in comparisons between different developmental stages in mice (R = 0.18) [7], between yeasts cultured on rich or minimal media (R = 0.45) [6], or between two murine hematopoetic cell lines (R = 0.59) [5], where the results for all detected genes were reported.
It has been reported in 6 -10% of infants with developmental delay [ 13] and 8-10% of mentally handicapped adults [ 6, 14].
Interestingly, this disadvantage of static cast shadows has also been reported in studies with humans in a developmental-cognitive context [[ 34], cf. [ 32]].
Two different chromosomal translocations associated with developmental dyslexia have been reported in two Finnish families (Nopola-Hemmi et al. 2000).
AVN has also been reported in young children undergoing arthroscopic reduction for developmental dysplasia of the hip (DDH).
Although clones and their nuclear donor animal have the same genome, developmental abnormalities have been reported in cloned mammals.
Mutations in the LTBP3 gene have already been reported in individuals with oligodontia (5), a dental developmental disorder defined by the absence of more than six permanent teeth.
A similar developmental delay has been reported in humans; as serum TCDD concentrations increase in either prenatal or premenarcheal samples, the timing of pubertal breast development is delayed (Den Hond et al. 2002; Leijs et al. 2008).
