In that case, one might predict that remediation of reading difficulties would involve a "normalization" of deficits in white matter structure.
Based on Halliday's function/rank matrix in Figure 8 above, we might predict that cohesion will be strongly associated with composing mode.
One might predict that, in such a situation, the lateralisation effect could be reversed to favour the left hemisphere.
If this were the case, one might predict that rasl11b knock down would rescue mesendodermal defects in other Nodal pathway mutants.
If that were true, one might predict that proteins that stimulate the immune response would be up-regulated among those animals that experienced a severe SCI event.
By this reasoning, we might predict that isolation by distance maintains the genetic differentiation we observed between Konkapot Creek and the Illinois sites.
Based on the observation that APL1A2 homozygotes are less susceptible and APL1A1/APL1A2 heterozygotes are more susceptible to P. berghei infection, one might predict that APL1A1 homozygotes would in turn be exceedingly susceptible for infection.
Indeed, one might predict that larger ring sizes would confer advantages in these cases.
Therefore, one might predict that auranofin could alter the cellular millieu to favoring apoptosis.
In this case we might predict that co-distributed peripheral endemics became isolated simultaneously in taxa with lower dispersal capability.
One might predict that strains bearing mutations in these enzymes would show similar phenotypes to sir2 mutants.
