The increase in prostaglandins may be explained by increased cyclooxygenase expression or increased cyclooxygenase catalytic activity.
This reduction can be explained by increased environmental stability and reveals the existence of structural variability within physiographic types.
To some, it has all the hallmarks of an epidemic; others say it can in large part be explained by increased public awareness.
Mutant coefficient of coincidence and crossover number phenotypes cannot be explained by increased DSBs or by prolongation of the crossover-designation stage.
The generally larger pores in the butyl-modified chitosan scaffolds might be explained by increased phase separation rates due to the introduced hydrophobicity of the chitosan polymer.
Such behavior could be explained by increased internal temperatures of specimens tested in air due to lower heat conductivity of air as compared to seawater.
Part of this association could be explained by increased risk of fatal ventricular arrhythmias [15].
However, the large increase in average achievement between cohorts might be explained by increased age, maturity, or familiarity with formal science assessments.
The observed splayed tips of axonemal microtubules could be explained by increased curvature of protofilaments that depolymerize [38].
Thus, the increase in glucose uptake with twitch-contraction presumably cannot be explained by increased AS160 phosphorylation.
Thus, the effects of pertussis toxin cannot be explained by increased or decreased colony growth, viability or pluripotency, but rather represent a disruption in colony morphology and organization.
