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Recent work has performed simultaneous PET-MR in [18F]FDG cases to examine cardiac viability (Nensa & Schlosser, 2014), cardiac sarcoma (Nensa et al., 2015) and active inflammation imaging of cardiac sarcoidosis (Schneider et al., 2014).
This technique can be used to accurately detect changes in cardiac viability following infarctions in small animal models [26].
It is important to point out that, in spite of the increase in cardiac viability in Th2.R cell recipients, such recipients did not have a reduction in the rejection score by standard histology criteria.
At day 14, there was a significant increase in cardiac viability (indicated by increased [18F]-FDG uptake) in the hESC-EC treated group compared to controls (26.3±1.8 vs. 22.4±3.4; P<0.05).
Cardiac viability was monitored by ATP levels in the hearts.
To determine the mechanisms of cardiac viability and I/R protection in hearts lacking Fh1, a critical component of the CAC, we applied a flux balance analysis (FBA) model of mitochondrial metabolism to predict the consequences of Fh1 depletion (Smith and Robinson, 2011).
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As conventional methods to preserve cardiac cell viability and contractile function following ischemia are limited in their efficacy, we developed a unique approach to protect the heart by transplanting respiration-competent mitochondria to the injured region.
For example, carbon nanotubes increase cardiomyocyte proliferation and maturation but do not change the cardiac fibroblast viability or proliferation [14, 15].
Cardiac myocytes viability was typically 70 to 80%.
In conclusion, the adoptive transfer of ex vivo generated, rapamycin-resistant host Th2-type cells represents an effective new approach to the prolongation of cardiac allograft viability.
The current study is the first to demonstrate that the adoptive transfer of Th2 polarized host T cells represents a candidate approach to prolong cardiac allograft viability.
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