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While the descriptive data indicate a small difference between patient purchase and nurse reports (10.3 vs. 12.4 months), the plates' qualitative data in Figure 1 indicate a far more complex discrepancy.
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This second discrepancy may be more complex since the disagreement between the simulation and the data concerns the steady-state level in acid phase, rather than the dynamics.
Connections designed more conservatively than members because they are more complex to analyze, and discrepancy between analysis and design is large.
The discrepancies become more complex when examining fast oscillations.
It is concluded that the removing of these discrepancies requires a more complex approach, the inclusion of the new physical mechanisms during the discharge (for example the magnetic field generated by the core current in the channel), that is a more accurate calculation of the channel discharge function.
Before discussing why this occurs we consider whether the discrepancies persist for more complex choices of the initial vascular network.
This discrepancy suggests that a more complex signaling pathway regulates p-4E-BP1.
This discrepancy may be explained by the more complex homeostasis of post-switch memory B cells.
However, an increasing number of publications indicate a more complex relation between the primary tumour and DTCs, with considerable discrepancies noted at the genomic level [ 12, 13].
As figure 2 shows, R values become smaller with the increase of model complexity as expected, a more complex model can describe genome composition more accurately, which results in smaller discrepancy.
The reasons for this discrepancy are unclear but may be related to differences in the more complex in vivo infection model that allows for more functional redundancy and is biologically more relevant.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com