Cerebrospinal fluid myeloperoxidase concentration and cerebrospinal fluid neutrophil count for all cases of encephalitis.

<p>Because at low levels neutrophils are just recorded as present or absent, and at higher levels actual counts are given we looked at CSF MPO concentrations using both these parameters. CSF neutrophil counts were given for 11 patients.</p

Concentrations of mediators in the CSF and serum of patients with encephalitis of immune-mediated, infectious and unknown aetiologies.

<p>Concentrations of mediators in the CSF and serum of patients with encephalitis of immune-mediated, infectious and unknown aetiologies.</p

The heatmaps give a visual representation of how closely concentrations of different mediators correlate in the samples by nearest neighbour correlation.

<p>Using a hierarchical cluster analysis the mediators are listed in the same order for each of the three aetiological groups to allow a visual comparison of the pattern between the groups. In the serum (a) the pattern of mediator correlations is similar for all three aetiological groups, where-as in the cerebrospinal fluid (b) the pattern differed between immune-mediated and infectious aetiologies, and the pattern for those of unknown aetiology is closer to that seen with infection.</p

Serum concentrations of mediators in patients with encephalitis of immune-mediated, infectious and unknown aetiology.

<p>Bars represent median concentration.</p

Baseline characteristics for all patients with Acute Encephalitis Syndrome eligible for study inclusion.

<p>Characteristics presented as number (%) or median (range).</p><p>AES, Acute Encephalitis Syndrome; No., number; GCS, modified Glasgow coma scale (score 3–15); LOS, Liverpool Outcome Score (1 [died] – 5 [no impairment]); na, not applicable.</p>*<p>Significant difference in the median age among patients Followed and Not Followed up, p = 0.029.</p>‡<p>Discharge GCS was not available for 3 patients who were followed up.</p>¶<p>Discharge LOS was not available for 25 patients (19 followed up and 6 not).</p

Educational and economic data among the 54 families interviewed, grouped by Liverpool Outcome Score.

<p>Results presented as number in each group with proportion (%) or Median (range) grouped by Liverpool outcome score (LOS) at follow-up; LOS 2 or 3 represents Severe or Moderate impairment; LOS 4 or 5 represents Mild or No Impairment; US$, United Sates Dollars.</p>*§‡<p>Significant difference in median values or proportion of patients between ‘LOS 2 or 3’ and ‘LOS 4 or 5’ groups (p = 0.048*, p = 0.004^§ and p = 0.007^‡ respectively). Significance measured via Mann Whitney U or Fisher's Exact Test.</p>†<p>15 participants provided specific information on admission medication cost.</p>¶<p>29 participants provided information on discharge medication costs.</p

Flow diagram of study participants' recruitment and follow-up.

<p>All children admitted to hospital fitting WHO criteria for AES who were alive at discharge were attempted to be followed-up (n = 96). Seventy-two families were successfully contacted. Among these families, six children had died and 1 declined to participate further. The remaining 66 children participated in follow-up.</p

Comparison of neurological impairment experienced by children with AES at discharge and at follow-up.

<p>Graph displays proportions (%) of the different types of neurological impairment experienced by children alive at discharge and at follow-up who had a Liverpool Outcome Score measured at both time-points (n = 50). Neurological impairment was identified by reviewing clinician based on the history. White bars; Problem at follow-up. Black bars; Problem at discharge. * Significant difference (P<0.05) in the proportion of children who exhibited a specific type of neurological impairment at discharge and at follow-up. Significance was measured by Fisher's exact test.</p

Comparison of neurological impairment experienced by children at follow-up classified with JE or ‘Other AES’.

<p>Graph displays proportions (%) of the different types of neurological impairment experienced by children that were alive at follow-up after hospitalisation with AES (n = 66). Children were classified as suffering from JE or ‘Other AES’ based on their anti-JE virus antibody titres measured during acute admission (see <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002383#s2" target="_blank">Methods</a>). Neurological impairment was identified by reviewing clinician based on the history. White bars; JE patients (n = 19). Black bars; ‘other AES’ patients (n = 47).</p

Gene expression of T-cell receptor signalling pathway and validation.

<p><b>A</b>. Transcripts that were SDE in TBM patients at admission compared to the 6 month time point that mapped to the T-cell receptor signalling pathway. After activation of the T-cell receptor, a cascade of signalling events is initiated leading to gene induction. Gene products highlighted green are significantly less abundant in TBM patients at admission compared to the 6 month time point. Corrected <i>p</i> value on Ingenuity Pathways Analysis = 1.47E^-11. Gene list provided in Tables D and E in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0185973#pone.0185973.s002" target="_blank">S1 File</a>. <b>B</b>. Validation of T-cell signalling pathway genes by RT-PCR in TBM patients (cohort 1). Selected genes in the T-cell signalling pathway were validated by RT-PCR including seven that were significantly less abundant at admission compared to post treatment (TRA, ZAP70, CD3G, CD3D, LAT, LCK, NFATC2) and one showing no change (NFATC3). Two genes were also included that were more abundant at admission compared to post treatment (AREG, SLC7A5) that acted as the positive controls. Fold change between TBM patients at admission and post treatment (n = 8) are shown relative to Beta actin control. Boxes show 25^th and 75^th percentile. Whiskers show lowest and highest data point and horizontal lines show medians. * <i>p</i><0.05, ** <i>p</i><0.01 shows significance using paired Wilcoxon rank test.</p