In this paper, we propose a QCA adder that shows significant fault-tolerance against all types of cell misplacement defects such as cell omission, cell displacement, cell misalignment and extra/additional cell deposition.
C2C12 myoblasts depleted of mATX3 by RNA interference exhibited a round morphology, cell misalignment, and a delay in differentiation following myogenesis induction.
Despite some increase of mATX3 levels at Day 3, comparing to Day 0 and Day 1, the Mjd siRNA cells still exhibited round shape, cell-cell misalignment and decreased amounts of α5 and α7 integrin subunits (Figure 4).
After induction of differentiation (Day 0 to Day 5), Mjd siRNA-transfected cells were phenotypically different from mock-transfected cells: cell shape was rounder, with very thin cell extensions and extensive cell-cell misalignment (Figure 2C).
Together, these results suggested that in the organ of Corti, lack of Prox1 function promotes some limited phenotypic alterations in the overall patterning resulting in a slightly disorganized distribution of supporting and hair cells, including short extra rows of outer hair cells and misalignment of inner hair cells.
This exposure also leads to atrophy that is characterized by specific targeting of glutaminergic and GABAergic precursor cells of the cerebellum (especially granule cells) resulting in misalignment of Purkinje cells and ectopic and multinucleated granule cells.
However, while Amb + Sal animals revealed normal scar morphology, tissues from HU + Sal animals had pockets of cell clusters, cellular misalignment, and misaligned collagen bundles oriented in separate directions creating discontinuities and voids within the matrix confirming a previous report [ 48].
Further analysis by CASC5 siRNA knockdown in HeLa cells revealed chromosomal misalignment and the premature entry of the cells into mitosis; this defect causes improper symmetrical and asymmetrical division, which results in inefficient proliferation, inappropriate neuronal number and abnormal brain size [ 45].
Manufacturing defects like the cell and concentrator misalignments are addressed and their impact on the overall performance are verified by numerical simulations.
In the new scheme only single phase cells are used, so there is no misalignment of cells.
Similar to the Nf1hGFAPCKO cerebellum in adulthood, disrupted patterning of GCs and Purkinje cells often co-existed with the misalignment of BG cells at P8. Indeed, all major defects observed in BG cells, GCs and Purkinje cells of the adult Nf1hGFAPCKO cerebellum were identified at P8, suggesting that these defects manifest during neonatal stages.
