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1 elopment for the treatment of hepatitis C or myocardial reperfusion injury.
2 ibution of nondiabetic and diabetic blood to myocardial reperfusion injury.
3 ity resulting in increased cytoprotection in myocardial reperfusion injury.
4 he protective functional phenotype of MIF in myocardial reperfusion injury.
5 uld prevent neutrophil activation and reduce myocardial reperfusion injury.
6 ming may not utilize ADO's potential against myocardial reperfusion injury.
7 ma has been shown to be cardioprotective for myocardial reperfusion injury and ischemia and may play
8 itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still
9 currently under investigation for preventing myocardial reperfusion injury have the potential to impr
10 associated with oxidative stress, including myocardial reperfusion injury, heart transplantation, st
11 l and antithrombotic properties that reduces myocardial reperfusion injury in animal models of myocar
12 itric oxide bioavailability, and ameliorated myocardial reperfusion injury in the setting of severe h
13 dings suggest that the blood contribution to myocardial reperfusion injury is amplified in diabetes.
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