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Again, surprisingly, mouse heart cells enlarged as they would in a well-conditioned athlete.
Transgenic expression of DN-Lats2 was used to inhibit endogenous Lats2 in the mouse heart.
Figure 1 Mouse heart MR (left) and fused with 18F-FDG static PET (right).
A single-shank microprobe was applied to the left ventricle of a mouse heart.
In vivo, Hph1 Hph1 dsRBD transferred and distributed ^ targeted siRNA throughout the whole mouse heart graft.
TGF-β overexpression in the mouse heart is associated with fibrosis and hypertrophy.
These commercially available devices are already small enough to fit inside a left-ventricle of a mouse heart.
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Sample SRR453174 (mouse heart RNA-seq) consisted of 82,886,668 x76bp reads as paired-ends.
Adult mouse heart was coronary perfused with collagenase, and ventricles were excised and further digested.
Figure 2 In vivo and ex vivo transversal tomographic images of an infarcted mouse-heart.
Overall, the results showed that ultrafine PM exposure increased ischemia reperfusion injury in the mouse heart.
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