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Dissecting Inflammatory Complications in Critically Injured Patients by Within-Patient Gene Expression Changes: A Longitudinal Clinical Genomics Study

Figure 6

ocMOF and gene expression dynamics of MHC-II and p38 MAPK.

For each ocMOF group, the dominant trajectory (thick colored line) was obtained by averaging all the standardized MHC-II (a) and p38 MAPK (d) probesets trajectories (gray lines) of patients within the ocMOF subgroup. Generally, the dominant trajectory for MHC-II increases with time for ocMOF i and ii, initially decreases and then increases for ocMOF iii, and decreases for ocMOF iv and v. For p38 MAPK, the early dominant trajectory decreases with time for ocMOF i and ii, initially increases and then decreases for ocMOF iii, and increases for ocMOF iv and v. The dominant trajectories within the first 100 h suggest that early expression changes (gray region) of MHC-II (b) and p38 MAPK (e) correlate with patient outcome. The number of up-regulated MHC-II (c) and p38 MAPK (f) probesets (computed using the two sampling time points closest to the 40–80 h post-injury interval) separates patients with ocMOF i, ii, and iii from patients with ocMOF iv and v (p-value of the Kruskal-Wallis test is 0.00004 for MHC-II and 0.00668 for p38 MAPK).

Figure 6