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Aptamers can control the biological functions of enzymes, thereby facilitating the development of novel biosensors. While aptamers that inhibit catalytic reactions of enzymes were found and used as signal transducers to sense target molecules in biosensors, no aptamers that amplify enzymatic activity have been identified. In this study, we report G-quadruplex (G4)-forming DNA aptamers that upregulate the peroxidase activity in myoglobin specifically for luminol.

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Myoglobin promotes nitrite-dependent mitochondrial S-nitrosation to mediate cytoprotection after hypoxia/reoxygenation.

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Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, 15261, USA; Department of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, 15261, USA. Electronic address:

It is well established that myoglobin supports mitochondrial respiration through the storage and transport of oxygen as well as through the scavenging of nitric oxide. However, during ischemia/reperfusion (I/R), myoglobin and mitochondria both propagate myocardial injury through the production of oxidants. Nitrite, an endogenous signaling molecule and dietary constituent, mediates potent cardioprotection after I/R and this effect relies on its interaction with both myoglobin and mitochondria.

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The clinical biologist plays a role as a consultant for the relevant use of biological examination. Advisory activities of the medical laboratory may help physician in diagnosis or therapeutic algorithm, avoiding redundant ordering or useless tests. In this context, we performed a review of literature about the clinically interest of myoglobin assays.

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Under acute hypoxic conditions, the muscle oxygen uptake (mV˙O) during exercise is reduced by the restriction in oxygen-supplied volume to the mitochondria within the peripheral tissue. This suggests the existence of a factor restricting the mV˙O under hypoxic conditions at the peripheral tissue level. Therefore, this study set out to test the hypothesis that the restriction in mV˙O is regulated by the net decrease in intracellular oxygen tension equilibrated with myoglobin oxygen saturation (∆PO) during muscle contraction under hypoxic conditions.

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