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Impaired function of isolated mitochondria in the presence of unlimited oxygen availability has been demonstrated earlier by our group [ 16] and by other workers [ 10], and can be explained with partial uncoupling of mitochondrial oxidative phosphorylation.
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Conversely, the lower percentages of encapsulation efficiency and NP yield obtained with PLA-PCL copolymer might be explained with a partial and fast precipitation of polymer that occurs after addition of organic phase to surfactant solution.
This difference can be explained with the only partial knockdown of Ubc9 (approximately 70%).
Delay in cataract development in Clock −/− mice compared with Bmal1 −/− mice can be explained by partial compensation of CLOCK function by NPAS2 or by the influence of multiple pathological changes in Bmal1 −/− mice.
In all, our data is consistent with decrease in H3K9me2, which could be explained by partial inhibition of SUVH4 activity.
This could be explained by partial deneddylation of Cul1 during the immunoprecipitation reaction.
These can be explained by partial inhibition of tubular transport of creatinine.
Thus the changing STx cytotoxicity profile with time might be explained by a partial recovery of functional organelles.
In light of our findings, these reports could be explained by a partial overlap of the medial and lateral divisions with the pmEC and the alEC, respectively.
This weak relationship might be explained by the partial volume effect in smaller tumors.
This may be explained by the partial formation of Zn x Cd1−xS alloy shells [22].
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