Additional file 2 of Pan-cancer landscape of aberrant DNA Methylation across childhood Cancers: Molecular Characteristics and Clinical relevance

Additional file 2: Supplementary Figure 1. A heatmap of correlations between SDMC methylation and gene transcription in adult cancers, colored by Pearson’s r. Only three SDMCs mapped to gene promoters are investigated. Associations with FDR values greater than 0.05 are shown as whit

Additional file 1 of Pan-cancer landscape of aberrant DNA Methylation across childhood Cancers: Molecular Characteristics and Clinical relevance

Additional file 1: Supplementary Table 1-7: Supplementary Table 1. Characteristics of methylation and gene expression data sets used in this study. Supplementary Table 2. Numbers of differentially methylated CpG sites identified in pediatric cancers. Supplementary Table 3. The list of SDMCs. Supplementary Table 4. Differentially methylated SDMCs in adult cancers. Supplementary Table 5. Co-location and enrichment of SDMCs in Genomic features. Supplementary Table 6. Associations between SDMCs and gene transcription. Supplementary Table 7. Pathway enrichment analysis of SDMCs

The change of metabolites involved in lipid metabolism.

<p>C57BL/6 mice were subjected to sham operation or 25 minutes of bilateral renal ischemia with 2 hours, 48 hours, and 1 week of reperfusion. The renal cortex, renal medulla and plasma samples were collected at sacrifice for metabolites profiling. The change of the metabolites was shown by box plots. (A) linolenate [alpha or gamma: (18∶3n3 or 6)] in plasma; (B) palmitoleate (16∶1n7) in plasma; (C) oleate (18∶1n9) in plasma; (D) acetylcamitine in plasma; (E) 3-hydroxybutyrate (BHBA) in plasma; (F) 2-palmitoylglycerophosphocholine* in plasma; (G) 1-stearoylglycerophosphoinositol in plasma; (H) glycerophosphorylcholine (GPC) in plasma; (I) glycerol in plasma; (J) 1-palmitoylglycerol (1-monopalmitin) in kidney; (K) 2-palmitoylglycerol (2-monopalmitin) in kidney; (L) sphingosine in kidney; (M) palmitoyl sphingomyelin in kidney; (N) palmitoyl sphingomyelin in plasma; (O) stearoyl sphingomyelin in plasma.</p

The change of metabolites involved in glucose metabolism and TCA cycle.

<p>C57BL/6 mice were subjected to sham operation or 25 minutes of bilateral renal ischemia with 2 hours, 48 hours, and 1 week of reperfusion. The renal cortex, renal medulla and plasma samples were collected at sacrifice for metabolites profiling. The change of the metabolites was shown by box plots. (A) glucose in kidney; (B) lactate in kidney; (C) succinate in kidney; (D) malate in kidney; (E) citrate in kidney; (F) glucose in plasma; (G) lactate in plasma; (H) succinate in plasma; (I) malate in plasma; (J) citrate in plasma; (K) fumarate in kidney; (L) acetyl CoA in kidney.</p

The metabolites of continuous inhibition in plasma after renal IRI.

<p>C57BL/6 mice were subjected to sham operation or 25 minutes of bilateral renal ischemia with 2 hours, 48 hours, and 1 week of reperfusion. The plasma samples were collected at sacrifice for metabolites profiling. The change of the metabolites was shown by box plots. (A) betaine; (B) glutamine; (C) methionine; (D) tyrosine; (E) proline; (F) gamma-glutamylalanine; (F) gamma-glutamylmethionine.</p

The change of metabolites involved in inflammation regulation.

<p>C57BL/6 mice were subjected to sham operation or 25 minutes of bilateral renal ischemia with 2 hours, 48 hours, and 1 week of reperfusion. The renal cortex, renal medulla and plasma samples were collected at sacrifice for metabolites profiling. The red colored numbers indicate statistically significant increase (P≤0.05). The green colored numbers indicate statistically significant decrease (P≤0.05). The blue colored numbers indicate narrowly missed statistical cutoff for significance (0.05</p

Hyperoxia-induced increase in Hsp70 expression is ROS-dependent.

<p>PAECs were treated with and without NAC (5 mM) and exposed to normoxia (nor) and hyperoxia (hyper) for 48 h after which Hsp70 protein level was measured. (A) Representative immunoblots of Hsp70. (B) Bar graph show the changes in Hsp70 protein levels quantified by scanning densitometry. Results are expressed as mean ± SE; n = 4. *<i>P</i><0.05 vs. normoxia; #<i>P</i><0.05 vs. hyperoxia+vehicle.</p

The global change of metabolites in ischemic acute kidney injury.

<p>Littermate C57BL/6 mice were subjected to sham operation or 25 minutes of bilateral renal ischemia with 2 hours, 48 hours, and 1 week of reperfusion. The renal cortex, renal medulla, and the plasma samples were collected at sacrifice for metabolites profiling. (A) The global change of metabolites in the kidney cortex; (B) The global change of metabolites in the kidney medulla; (C) The global change of metabolites in the plasma; (D) The heat map of the metabolites in the kidney cortex and medulla; (E) The heat map of the metabolites in the plasma.</p

Hyperoxia increases Hsp70 expression.

<p>PAECs were exposed to normoxia (room air, 5% CO₂) or to hyperoxia (95% oxygen, 5% CO₂) for 1 to 24 h or 48 h after which the protein and mRNA levels of Hsp70 were measured. (A) Representative immunoblots of Hsp70. (B) Bar graph show the changes in Hsp70 protein levels quantified by scanning densitometry. (C) Bar graph showing the changes in the mRNA levels of hspA1A, hspA1B and hspA2 quantified by quantitative real-time PCR. Results are expressed as mean ± SE; n = 4. *<i>P</i><0.05 vs. normoxia.</p

The metabolites of continuous inhibition in kidney during renal IRI.

<p>C57BL/6 mice were subjected to sham operation or 25 minutes of bilateral renal ischemia with 2 hours, 48 hours, and 1 week of reperfusion. The renal cortex and renal medulla were collected at sacrifice for metabolites profiling. The change of the metabolites was shown by box plots. (A) betaine; (B) Isobar: betaine aldehyde, N-methyldiethanolamine; (C) glutamate; (D) glutamine; (E) 5-oxoproline; (F) adenosine 5′-monophosphate (AMP); (G) inosine; (H) ribitol; (I) nicotinamide; (J) succiylcarnitine.</p