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However, several recent studies have raised reservations over the measurement of ROS production in vitro [ 8– 10], since artificially high levels of metabolic substrates [ 11] and very high partial pressures of oxygen (20% in contrast to approx. 5% in vivo [ 10]) make extrapolations of in vitro results to the in vivo situation potentially problematic [ 7, 8].
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While this phantom represented our best available vascular access model, the differences with human tissue and the location of deeper vessels make extrapolation of this study difficult in a live human setting.
Several factors make extrapolation of H2O2 production by isolated mitochondria to the in vivo situation invalid.
This variation makes extrapolations of therapeutic concentrations between species difficult.
Second, in making extrapolations of bacteremia rates, we made some assumptions that could have biased our adjusted rates.
The study population was homogenous including only elderly men living within a geographically limited area, so one should be cautious about making extrapolations of these results to other population groups.
As higher order zeta diversity is only a subset of lower order ones, this declining trend constrains the variation of zeta diversity at higher orders and in turn makes extrapolation of higher order zeta diversity less problematic.
However, scaling fluidized beds for dynamic similarity continues to be challenging because flow hydrodynamics at lab-scale are largely influenced by bed geometry making extrapolation of conclusions to large-scales infeasible.
Therefore, in vitro culture conditions for S. aureus and those in vivo are likely much different, making extrapolation of in vitro results with animal infections models less predictable.
All patients in the present study were aged between 72 and 85 years, which makes extrapolation of our results to younger individuals arbitrary.
First, there was significant heterogeneity in the studies, making extrapolation of conclusions fraught with error.
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