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Genome-wide expression analysis solved this pro-cardiac phenotype in relationship with bona fide cardiomyocytes, and evidenced the underlying activated pathways of pro-cardiac to cardiac determination [16].
Accordingly, targeted treatment with SDF-1, VEGF, and BMP2 was designed to activate predicted network hubs, a strategy that effectively accelerated cardiac determination.
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Conclusion: In patients undergoing cardiac surgery, determination of ITBVI* revealed close agreement with measurements derived by ITBVI.
Figure 3 Relationship between percent changes in cardiac index determination using ECOM (ΔCI PC ) and cardiac index determination using pulse contour analysis (ΔCI ECOM ) following fluid challenge in 25 patients (25 paired data points).
CIECOM = cardiac index determination using ECOM (L.min-1.m-2); CIPC = cardiac index determination using pulse contour analysis (L.min-1.m-2).
CIECOM = cardiac index determination using ECOM (L.min-1.m-2); CIPC = cardiac index determination using pulse contour analysis (L.min-1.m-2); PLR = passive leg raising.
A cardiac output determination using the thermodilution technique was also made at this time.
Cardiac output determination by thermodilution has been developed in adults using a pulmonary artery catheter (Pulmonary Arterial ThermoDilution).
Cardiac output determination by thermodilution/pulse contour analysis using a PICCO®-type system may be considered in patients with cardiogenic shock refractory to first-line treatment (strong agreement).
Results of further investigations using spinal magnetic resonance imaging, intravenous pyelography, renal CT, cardiac enzyme determination were within their normal ranges.
In this process, morphogenic movements and cardiac fate determination are regulated by cytokines such as bone morphogenetic proteins (BMPs) [1] [3], and fibroblast growth factors (FGFs) [4] [7].
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