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Alternatively, we might expect increased growth due to enhanced activity of the oncogene.
Alternatively we might expect the tip scanning to influence a putative sliding process but such a phenomenon was never observed.
Alternatively, one might expect that orthologous loci in other species could be diverse regardless of their role in host specificity.
Alternatively, we might have expected transplanted cells to mediate recovery by increased sparing of white matter around the lesion [68].
Alternatively, it might be expected that some channels and transporters poorly distinguish between K+ and NH4+.
Alternatively, metformin might be expected to block an essential senescence escape mechanism while nullifying EMT-driven CSC features by preventing molecular transition of epithelial tumour cells to embryonic mesenchymal phenotypes (i.e. EMT) [ 35- 38].
So what might we expect?
One might therefore expect a certain stridency.
Alternatively, if RDR2 were to act upstream of Pol IV, which is contrary to current models, but a formal possibility, one might similarly expect to detect RDR2 transcripts in a pol IV mutant.
Alternatively, if the distal O were protonated first, one might expect to observe formation of an inner-sphere peroxo intermediate as observed for MnSOD (see section 5).
Alternatively, if dedifferentiation programmes can be faithfully re-initiated, then one might expect a constant ability to regenerate, though perhaps not a perfect regeneration response.
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