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These results could be explained by reduced fertilization success of cryopreserved sperm.
Mechanistically, reductions in mitochondrial oxygen consumption and H2O2 generation triggered by a blood meal could be explained by reduced electron flow in the ETC produced by either diminished mitochondrial substrate uptake [58] and/or oxidation.
This mortality benefit may partially be explained by reduced risk.
In cells deficient in Leo1 Paf1, the increase that we observe in H3K9me2 can be explained by reduced histone turnover.
The resistance of these clones could be explained by reduced drug accumulation and was associated with a decrease rather than an increase in the low MDR1 mRNA level.
Overall, five studies have found higher mortality rates in cancer patients with previous SCC [ 4, 10- 13], which also could be explained by reduced immune competence.
These findings may be explained by reduced oxygen transportation from the mother to fetus and may reflect inadequate iron reserves during early pregnancy.
The non-sustainable response to therapy could also be explained by reduced drug levels over time as shown in pharmacokinetic studies of GIST patients wherein imatinib levels decrease with ongoing use because of increased drug clearance (Judson et al, 2005).
In the present study, significantly decreased NAGase (Tables 2 and 4) could be explained by reduced milk SCC which could be due to declined IMIs following RAMP-O treatment.
The higher concentrations of malic acid, K+ and other inorganic ions detected in sap of Li 1 – Li 2 can be explained by reduced influx of water into fiber cells of mutants.
This may in part be explained by reduced food intake because of impaired autonomy, eating disturbances and reduced appetite.
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