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nNOS-deficiency caused reductions in skeletal muscle bulk and maximum tetanic force production in male mice only.
The maximum tetanic force generated immediately prior to the initiation of the subsequent lengthening contraction was recorded and normalized.
nNOSμ-deficiency significantly reduces skeletal muscle mass, maximum tetanic force output and fatigue resistance; therefore qualifying the skeletal muscles of KN1 mice as myopathic.
As in the experiments described above, TA muscles in the GarsC201R/+ mice were significantly weaker and had a maximum tetanic force of 60.6±3.0 g (P = 0.002).
Maximum tetanic force was significantly decreased in KN1 male TA muscles only (Figure 2A), paralleling the decreases in muscle mass described above.
The maximum tetanic force was decreased in Akt1ko and Akt2ko (Figure 7C, p<0.01), but tetanus dynamics were not different (Figure 7D).
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Given the reduced TA muscle bulk in male KN1 mice, we tested whether the maximum tetanic force-generating capacity of nNOSμ-deficient TA muscles was also decreased (Figure 2).
Main Outcome Measures: Extensor digitorum longus maximum isometric tetanic force (Po) was measured in vitro from all extensor digitorum longus muscles and used as a functional index of muscle injury.
The muscle specific force at optimum length was expressed as the maximum isometric tetanic force per unit cross-sectional area of muscle.
Muscle contractile properties were tested in terms of muscle specific force, which was measured at 25°C and calculated by dividing maximum isometric tetanic force by mean muscle cross-sectional area.
Maximum isometric tetanic force (Fo) was calculated from the resulting sets of recorded force traces.
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