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By this hypothesis, the starting point of Pax4 activation for β-cell differentiation is downstream of endodermal pancreatic induction itself, so that Pax4 activation affects pancreatic endocrine cells that spontaneously differentiated from endoderm in EBs, while other 'lineage-precommitted' stem cells are not responsive.
By this hypothesis, higher biomass loadings are effectively increasing the severity of the AHP pretreatment (due to the increased molar concentration of H2O2 and NaOH), leading to progressively greater cellulose susceptibility to CBH.
By this hypothesis, the levels of in utero/perinatal mitogens and other factors determine the size of the stem cell pools in the developing fetus; elevated tissue stem cell numbers drive the formation of larger organs and hence might be associated with larger birth weights.
The K T mass extinctions, however, do not seem to be fully explained by this hypothesis.
Thus, by this hypothesis, we get.
Several macroscopic structures in the deformed Opx can be accounted for by this hypothesis (Figure 9).
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By addressing this hypothesis, we aimed to elucidate the neural mechanisms underlying motion sickness in humans.
Let us begin by reviewing this hypothesis.
Several genes from our microarray results suggest directions by which this hypothesis could be tested.
Though backed by theoretical considerations, this hypothesis has hardly been tested empirically.
Reactions by others to this hypothesis sometimes claimed that such an explanation was simply absurd.
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CEO of Professional Science Editing for Scientists @ prosciediting.com