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All the test defects showed complete osseous healing after 90 days compared to those in the control defect.
During the observation period, no significant differences in BV/TV and mineralization of newly formed bone among the test defects were observed.
In the early stages of wound healing, up to 30 days, the test defects did not show better bone regeneration than those in the control defect, but the bone healing process in the test defects was accelerated in the later stage compared to those in the control defect.
This is increased by organizational and software technical dependencies (new built functionality; technical, testing, defect, integration debts).
One of the most significant (p < 0.05, Student's t-test) defect is the ability to split pseudopods: the ratio of newly generated pseudopods arising from splits decreases 27% and the splitting rate decreases 36%.
Figure 8 Fatigue test, showing defect propagation.
The results of other tests on defect removal are shown in Figure 13.
The biomechanical testing showed defect gap alterations between 0.03 mm and 0.22 mm for the applied scaffolds and 0.09 mm for the intact bone.
To test for defects in Bmp signaling, we investigated the expression of phosphorylated Smads1, 4 and 8.
Such localized deformation and shear failure was previously reported during in situ SEM tensile testing of defect free (111) oriented Cu whiskers in a similar size range.
Therefore, we wanted to test whether defects in Ku– TLC1 interaction alone affects the ability of a Cdc13– Est1 fusion to promote progressive telomere elongation.
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CEO of Professional Science Editing for Scientists @ prosciediting.com