Sentence examples for migration abnormalities in from inspiring English sources

Migration abnormalities in other fragments containing exons 4 and 6 and introns 3 and 9 were detected in 2, 23, 4 and 4 patients, respectively.

DGGE analysis of exons 4 9 of the p53 gene revealed consistent migration abnormalities in 167 fragments; 134 of these fragments were shown to be the Arg72Pro polymorphism (see below).

Interest in neuronal migration in the cerebral cortex has never been greater, because investigations into the mechanisms that regulate neuronal movement pointed to migration abnormalities in several naturally occurring genetic defects in humans (Ross and Walsh, 2001).

Consistent migration abnormalities were noted in 167 fragments, 134 of which were shown to be the Arg72Pro polymorphism, whereas migration abnormalities in fragments containing exons 4 (n=2) and 6 (n=23) and introns 3 (n=4) and 9 (n=4) corresponded to five previously described polymorphisms.

Although Dcx-cre-mediated deletion of mTOR did not show migration abnormality in the cerebral cortex, we cannot exclude the possibility that mTOR has a role for neuronal migration and subsequent positioning in the developing brain.

As Reelin is expressed in the developing hilar region adjacent to the CA3 area when EphB1/EphB2-expressing neural precursors are actively migrating to the same hippocampal location, it seems plausible that the lack of Reelin-mediated EphB forward signaling results in the specific CA3 migration abnormalities observed in EphB1/2-deficient mice.

In contrast, targeting both neurons and glia for DG deletion during embryonic development results in widespread, yet heterogeneous GC migration abnormalities without reducing overall cerebellar growth.

In PDE cortex, antiquitin immunofluorescence was greatly attenuated with evidence of perinuclear accumulation in astrocytes.Antiquitin is expressed within glial cells in the brain, and its dysfunction in PDE is associated with neuronal migration abnormalities and other structural brain defects.

Collectively, this pathology is responsible for the granule cell migration abnormalities observed here and may be largely responsible for the cerebellar dysplasia observed in dystroglycanopathy patients.

Peñagarikano, O. et al. Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities and core autism-related deficits.

This form of cortical dysplasia is due most probably to neuronal migration abnormalities during development [7].