Birefringence imaging and statistical analyses of the numbers of embryos with normal and abnormal muscles after APM treatments demonstrated that at 0.3 and 0.5 μM APM, there is a highly significant elevated susceptibility of capn3b −/− embryos to muscle damage due to hyperactivation by AchE inhibition, whereas in the control media both types of embryos are normal, and at 0.75 μM APM they both have similar rates of abnormal muscles ( Figure 6 B).
← all excerpts
Loss of <i>calpain3b</i> in Zebrafish, a Model of Limb-Girdle Muscular Dystrophy, Increases Susceptibility to Muscle Defects Due to Elevated Muscle Activity.
1
—
—