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In contrast, and consistent with data from mouse ventricular CMs, we observed that GLP-1(2836) failed to protect hESC-CMs from cytotoxicity under conditions of oxidative stress (Supplemental Figure 4C)

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Second, we hypothesized that chronic, exogenous activation of this excitatory pathway could reverse the crossed cerebellar diaschisis, and possibly even atrophic changes, that occur following contralateral cortical ischemia and contribute to loss of function [90, 94, 120]