To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
In mdx mice, a model for Duchenne muscular dystrophy, the timing between the replication of myoblasts
and their incorporation into myotubes was determined autoradiographically. Thirty-eight mdx mice aged
23 d were injected with tritiated thymidine to label myoblasts replicating early in the dystrophic process. At
intervals from 8 h to 30 d after injection the tibialis anterior muscles were removed, processed for
autoradiography and analysed for labelled central myonuclei (derived from the progeny of myoblasts which
had been labelled at 23 d). At 8 h after injection there were no labelled central myonuclei, showing that the
labelled myoblasts had not fused within this time. At 1 d, 2% of central myonuclei were labelled, at 2 d, up
to 32% were labelled, at 3 d ∼60% were labelled, and at 4 d the labelling peaked at 74%. In the 27 mice
sampled from 5–30 d after injection, the levels of central myonuclear labelling varied enormously: from
1–63%. However, there was a consistent decrease in the numbers of labelled central myonuclei with time.
This may have been due to dilution of the relative numbers of labelled myonuclei due to other, nonlabelled,
myoblasts replicating after the availability of tritiated thymidine, and fusing. It was also possible that
labelled myofibres underwent subsequent necrosis and were eliminated from the muscle. The proposal that a
regenerated myofibre can undergo a subsequent cycle of necrosis and regeneration was supported by
evidence of some necrotic myofibres with labelled and unlabelled central nuclei. These results have
implications for understanding the cellular biology and pathology of dystrophic muscle, particularly in
relation to myoblast transfer therapy as a potential treatment of Duchenne muscular dystrophy.
The difference in the timing of the regeneration process of skeletal
muscle between SJL/J and BALB/c mice
was investigated using grafts of whole skeletal muscle (both autografts
autoradiographic and immunohistochemical techniques were used in the
investigation. Infiltration of
leucocytes into autografts, numbers of desmin-positive myogenic cells and
myotube formation were all more
advanced in the SJL/J compared with BALB/c mice. Furthermore,
autoradiographic evidence showed that
myoblasts in the SJL/J autografts were synthesising DNA 12 h earlier
than myoblasts in BALB/c
autografts. In allografts, where SJL/J host mice received BALB/c
grafts, and vice versa, leucocyte
infiltration and myotube formation occurred earlier in the BALB/c muscles
grafted into SJL/J hosts, than
in the reverse situation with BALB/c hosts. The results show that,
least for whole muscle grafts, it is the
host environment which determines the speed and outcome of the regenerative
Email your librarian or administrator to recommend adding this to your organisation's collection.