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During the stretching of unit I of the dimer in either type of the experiments mentioned above, we occasionally observed a force peak having the force of about 0.5 0.7 nN when extension length reached 40 50 nm.
We observed a force plateau followed by a steep increase in force at larger extensions.
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In apparent contrast, we observed a decreased force in single fibers after 18 hours of hypercapnic mechanical ventilation.
In support of the first possibility, we observed a significant force decline in many of the electrically stimulated muscles i.e., some muscles showed a decline in peak tension development of more than 25% by the end of 1 hr. of stimulation.
The probability density function (pdf)(56) of 199 unbinding events shows the expected average avidin biotin rupture force, as previously observed a the same force loading rate.
The active force was determined by subtracting the average resting force (measured before and after activation) from the total force, observed as a force plateau at each activation.
A significant increase was observed when a force of 3 N was applied 1 and 2 N being ineffective.
When increasing the compressive force of MLL, we observed a 33% increase in transverse force at a frequency of 0.25 Hz and a 43% increase in transverse force at a frequency of 0.5 Hz.
We observed a plateau in the force measurements between the PEG-modified tip and the TiO2 (110) surface (Fig. 8a, b).
When αSMA was depleted in human CAFs, we observed a loss in contractile force as measured by contraction of collagen matrices (Fig 3F).
Regarding the post-fatigue tetanic and specific forces, we observed a reduction in tetanic and specific forces in injured TA muscles from WT and β2KO mice when compared to their controls (WT mice: 42 and 40% respectively; β2KO mice: 43 and 24% respectively; P ≤ 0.05, Fig. 9).
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