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Of note, there is a high rate of viral persistence in the myocardium of patients with idiopathic DCM [ 92].
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This is confirmed by the fact that in patients with clinically suspected DCM with a chronic progression of LV dysfunction, viral persistence in the myocardium (Fig. 4) as well as myocardial inflammation (Fig. 5) can be detected in a high percentage in these patients [ 29, 31, 32, 47, 48, 50, 52].
PKD and ER stress were excessive activated in the myocardium of diabetic rats.
Viral infection in the myocardium of American and Japanese patients with end-stage IDC was evaluated.
It is possible that the greater levels of pro-inflammatory cytokines in the myocardium of old mice are due to chemokine-mediated leukocyte accumulation in the myocardium.
In WT hearts, widespread CENP-F expression is observed throughout the myocardium (Fig. 1E,F), whereas expression is absent in the myocardium of CENP-F −/− mice (Fig. 1G,H).
GLP-1 has been shown to enhance glucose uptake in the myocardium of isolated rat hearts and in dog myocardium [ 11, 12].
These observations are in agreement with molecular changes occurring in the myocardium of ARVC patients.
Serine phosphorylation of Akt (serine 473) was impaired in the myocardium of db/db mice.
Protein levels of NF-κB p65 were markedly increased in the myocardium of db/db mice.
PICALM antibody positivity was identified in the ridge and the myocardium of all dogs including the myocardium of the control beagle, demonstrating its presence in myocardium and LVOT.
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