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A trivial explanation for the gene length dependent effects we have observed in ORFs would be that gene regulation during stress adaptation is correlated with gene length.
Although a trivial explanation, the interaction strength between the nanotube and underlying substrate, which changes the value of COF for several times, has a drastic influence on the use of nanomaterials as lubricants.
Therefore, compensatory paired 454 errors could be a trivial explanation of these odd V3 sequences.
A laboratory error in the IFN γ detection is a trivial explanation that cannot be ruled out.
Again, the trivial explanation is that this is due to an increase in the rate of synaptic input.
A trivial explanation for doxycycline-independent tumor viability could be either the aberrant expression of MYC independent of doxycycline or endogenous upregulation of murine c-Myc.
Although unlikely, a trivial explanation for these findings is that LA is not bound to HNF4α within cells, but becomes associated with the receptor after lysis.
This latter observation might have a simple or trivial explanation, such as biases in AT vs. GC content or chance occurrence related to taxon sampling.
A trivial explanation is that the increase in network activity increases the rate of synaptic input to the neuron, reducing its Rin.
However, a trivial explanation for ouabain-resistance of ankyrin-B+/− mice could be that chronic elevation of [Ca2+]i transients in ankyrin-B+/− cardiomyocytes caused compensatory adaptations.
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While the trivial explanation of these findings could have been that the intronic regions simply follow the change of the corresponding mature RNAs (the exons), relatively few loci followed this pattern.
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