Sentence examples for responsiveness to loading from inspiring English sources

The rationale for examining the bone loss associated with disuse in these groups of mice was our hypothesis that if a more robust skeletal phenotype is a result of greater responsiveness to loading then the degree of bone loss associated with removal of the loading-related stimulus should also be greater.

However, the effect of gender on the skeletal responsiveness to loading has been previously assessed [16], [17], [62] [66], suggesting that males are more responsive to loading than females.

In contrast, the tibias of male and female mice heterozygous for the Lrp5 G171V HBM mutation showed greater osteogenic responsiveness to loading and less bone loss associated with disuse than their WT HBM− controls.

Our hypothesis was that high responsiveness to loading would be associated with increased bone loss due to disuse and a steep "responsiveness" curve between strain magnitude and the increase in new bone formation.

Conversely if a less robust skeletal phenotype were to be due to a lower osteogenic responsiveness to loading this should be reflected by a lower level of bone loss associated with disuse.

In contrast, the presence of the Lrp5 G171V HBM mutation in both males and females was associated with some protection against disuse-related bone loss in both cortical and cancellous bone and an increased osteogenic responsiveness to loading that was especially apparent in the females.

The rationale for examining the osteogenic response to loading was to assess more directly the potential role of Lrp5 in bone's responsiveness to mechanical loading.

Assessment of SVV and ITBI on the responsiveness to volume loading were more useful indicators than HR, MAP, CVP, and PAWP.

To assess the significance of stroke volume variation and intrathoracic blood volume index on the responsiveness to volume loading in canines with hemorrhagic shock.

The data we present here, at least in male mice, are consistent with the differences in bone mass between normal WT mice and those that lack Lrp5 function, being due to an altered responsiveness to bone loading.

In conclusion, the data presented here indicate that the expression of the human Lrp5 G171V HBM mutation is associated in both cortical and cancellous bone with an increased osteogenic responsiveness to supra-physiological loading, which is more marked in females than males, and with some protection against the bone loss associated with neurectomy-induced disuse.