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The cultured strips of cardiac cells generate physiologic calcium transients and twitch force, and respond to electrical pacing and adrenergic stimulation.
No difference was observed between AV.RSV.MCAT infected mice and uninfected controls in terms of twitch force, tetanic force, fatigue pattern and eccentric contraction response (Figure 4).
Long periods of stabilization were avoided to prevent muscle run-down of twitch force [ 20].
Force frequency relationships revealed significantly reduced twitch force amplitudes in TG papillary muscles.
Compared to non-transfected muscle, twitch force (-12%) and maximal tetanic force (-30%) were reduced and time-to-peak-twitch force (+22%) and half-relaxation-time (+32%) were prolonged in control-transfected muscle (Table 1).
This was dose-dependent, induced nearly complete inhibition of twitch force at high-doses and was partially reversible.
At 10−4 M 8-bromo cGMP twitch force and FTI reached were minimal with reduction by 28±6%6% and 37 ± 8% respectively (both P < 0.01).
Significant increases in the temporal parameters of contraction and relaxation in twitch force after rewarming likely reflect a change in myosin/actin cross-bridge cycling kinetics.
A sliding window of 7 ms width was advanced in steps of 1 ms throughout each steady-state length and twitch force profile.
Half-relaxation time was measured from the peak of twitch force to the point where twitch tension fell to half of its peak value.
One study found that the soleus muscle of dystrophin-utrophin double knockout mice had a greater reduction in twitch force than in extensor digitorum longus and diaphragm [ 47].
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