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The model of muscle breakdown/atrophy was the gastrocnemius muscle denervation model described previously [ 16, 17].
The present study is the first in which BM transplantation in a human muscle denervation model was assessed with objective measurements (histology, CT muscle and EMG).
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Here, we show abnormal expression of the myogenic program in primary myoblasts from Smn 2B/− mice and in vivo, where we demonstrate the presence of delayed skeletal muscle development independent of myofiber degeneration and muscle denervation in mouse models of SMA.
To assess Smad induction in non-ALS muscle denervation, we used a model of sciatic nerve injury.
To investigate whether Pax7 and MyoD levels could change following muscle denervation, we experimentally denervated wild-type mice.
Laceration consists in a deep cut across the muscle [ 87] which causes a delay in the healing process, while the denervation model involves severing the sciatic nerve, thus causing atrophy of the denervated myofibers [ 88].
The TA muscle was selected as it is spared from histological denervation in mouse models of SMA and therefore it would likely not be influenced by muscle denervation induced atrophy (29, 30).
This model recapitulates many of the pathological and clinical features of ALS, including progressive weakness, motor neuron loss, and muscle denervation.
To determine the relationship among spinal stenosis, back pain, paraspinal muscle denervation, and paraspinal muscle atrophy.
Detection of MR signs of muscle denervation should be regarded as indicative of surgical nerve decompression.
MR signs of muscle denervation within the anterior compartment are important secondary signs for evaluation of the peroneal nerve.
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