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Fig 1.

Study outline of analyses to uncover unique gene expression patterns underlying IVIG responsiveness in subjects with elevated serum GGT levels.

(1) Analysis of GGT levels with IVIG responsive-ness; (2) Global gene expression analysis by R2 statistic and FDR anal-yses to identify genes, explaining variations in both IVIG responsiveness and GGT elevation; (3) Targeted analysis of the step 2 discovered genes in either GGT normal or elevated subgroups to reveal gene expression patterns specific for each sub-group of subjects; (4) Pathway and literature analysis to explore the underlying biology of IVIG resistance in subjects with GGT elevation.

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Fig 1 Expand

Table 1.

Clinical and laboratory characteristics values of 686 IVIG responsive and resistant KD subjects.

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Table 1 Expand

Fig 2.

Odds ratio for IVIG resistance per quintile of GGT level.

The odds ratios were calculated against the first quintile with the lowest GGT level. The 95% confidential intervals were shown as the error bars. **: P value < 0.01 using fisher exact test.

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Fig 2 Expand

Fig 3.

R2 statistic and FDR analyses with respect to GGT levels and IVIG responsiveness.

Top left panel: discovery of genes explaining variations in IVIG responsiveness. Top right panel: discovery of genes explaining variations in GGT levels. Bottom panel: Venn diagram analysis uncovering genes explaining variations in both IVIG responsiveness and GGT levels.

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Fig 3 Expand

Table 2.

List of 12 genes significantly contributing to IVIG resistance in subgroup with elevated GGT levels identified by logistic regression from 36 genes found by R2 statistic and FDR analyses.

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Table 2 Expand

Fig 4.

Neutrophil reduction in response to IVIG treatment in two independent cohorts.

All P values were calculated using Wilcoxon rank sum test. A) Cohort III. B) Cohort IV. The number of patients with rising neutrophil counts after IVIG treatment were indicated by the numbers below x axis alongside each box plot. The P values were calculated using Wilcoxon rank sum test.

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Fig 5.

Hypothesis of the underlying biology of IVIG responsiveness involving neutrophils, siglec-9, ST6GALNAC3, and GGT.

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Fig 5 Expand