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In summary, the myocardium does not experience the same reductions in protein content that are characteristically observed in skeletal muscle following continuous LPS administration.
In summary, these findings suggest that the myocardium does not undergo the same catabolic response as skeletal muscle during early endotoxaemia, partly due to the absence of transcriptional and signalling events in the myocardium typically associated with increased muscle proteolysis and the suppression of protein synthesis.
Moreover, the presence of vector DNA in the myocardium does not necessarily imply bona fide gene transduction.
Myocardial ischemia occurs when the myocardium does not receive sufficient blood flow, resulting in irreversible injury and cell death [ 65].
And, strikingly, only one layer of the two-ply heart, the pericardium, expresses Pax2/5/8b; the muscular myocardium does not.
Normal myocardium does not enhance because extracellular magnetic resonance contrast agents, such as Gd-DTPA, are excluded from the myocyte intracellular space by intact sarcolemmal membranes and also, little interstitial space is available between densely packed myocytes [ 60].
Similar(54)
In stark contrast to the EDL, the myocardium did not display altered mRNA levels for either MAFbx/atrogin-1 or MuRF1 following LPS administration at any of the three time-points examined (Fig. 3A & 3B).
The myocardium did not show notable inflammation or necrosis.
The collagen content of the myocardium did not correlate with total recoverable collagen.
Remote myocardium did not display LGE and was in a different myocardial territory than the infarction.
Absolute perfusion under adenosine of the global left-ventricular myocardium did not change under therapy or minimal coronary resistance.
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