Figure 1.
Lactate concentrations (A) and partial pressure of oxygen (B) over the whole course of the experiment. Mean and 95% confidence intervals are given for the LPS (thick line) and the control (dashed line) groups (n = 7 (control)/9 (LPS) +q0.2; *, q
0.05; **, q
0.001).
Table 1.
Description of the cohort.
Figure 2.
Metabolite response to LPS in the acute phase.
Cluster analysis of the time courses for the metabolites altered in the LPS cohort within the first 3 days. Left: display of the time courses for 3 groups of metabolites altered in the LPS cohort within the first 3 days. Middle: dendrogram from the hierachical clustering (HCA), based on the absolute value of the correlation between coefficients of the linear model. Right: explicit display of each metabolite time course for each cluster identified by HCA. The average time course is plotted as a dashed line.
Figure 3.
Metabolites altered by LPS after the acute phase.
Fold changes (log basis 2) for the metabolites altered at FDR0.1 at any time point after 4 days. Abbreviations: ADMA/SDMA, Asymmetric/symmetric dimethylarginine; Total DMA, sum of ADMA and SDMA; DHA, Docosahexaenoic acid. Significance: + = q
0.2, * = q
0.05, ** = q
0.001.
Figure 4.
Correlation between metabolites and brain damage.
Heatmap depicting metabolite association with white matter and grey matter volumes during the acute phase (6–48 h) and late phase (6–9 days). Color coding follows the key (top right): blue (resp. red) correspond to positive (resp. negative) correlation with the white and gray matter volume (red: increase in metabolite concentration correlates with maldevelopment, blue: decrease in metabolite concentration correlates with maldevelopment, the darker the stronger the correlation). Light grey corresponds to metabolites that were not found to be significant at FDR0.1.
Table 2.
Roles and functions of a selection of altered metabolites.