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We reconstructed a mean heart model and studied its sensitivity to specific lipid profiles.
The analysis was performed for each surface point by regressing the lipid profiles to the heart surface models' deviations from the mean heart model.
Projection of the lipid change onto the surface normal of the mean heart model was accompanied with the decrease in wall thickening and motion in septum.
The change in the heart model was visually evaluated by computing the wall thickening and/or wall motion from end-diastolic shape to end-systolic shape and visualizing the results using color maps overlaid on the mean heart model.
To regularize the analysis, only the deviations on mean heart model's surface normal were studied.
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Dependent variables for this model included: pre-test anxiety level, mean heart rate, peak heart rate, and PGY status (see Table 1 for full model specifications).
Since the mean heart rate is not constant (it evolves continuously in challenging situations, such as physical and mental effort, especially in critically ill patients), the HRV signal was corrected by the time-varying mean heart rate [33], yielding the modulating signal which, according to the IPFM model, represents autonomic nervous system modulation over the sinoatrial node.
Model: Ottawa Overall Score = β 0 + β 1 (pre-test anxiety level) + β 2 (mean heart rate) + β 3 (peak heart rate) + β 4 (PGY status) + e. Adjusted R-square for model = 0.16; F = 2.48; P = 0.07.
Using SFS, 6 out of the original 24 physiological variables were chosen: mean heart rate, mean temperature, mean platelets, mean blood pressure, mean SpO2, and mean lactic acid.
Peak heart rate and mean heart rate showed similar relationships.
Her mean heart rate was 60 70 beats/min.
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