Kaplan Meier failure curve, all patients.

<p>Kaplan Meier failure curve, all patients.</p

FuSAM study flow chart - all admissions to MOYO.

<p>(OTP = ‘Outpatient Treatment Programme’ – the outpatient part of treatment; T/F = transfer out to different programme). ‘Still sick’ children were seen or reported to be clinically unwell at follow-up but details were not always known.</p

Boxplot showing weight-for-height, weight-for-age and height-for-age of the ex-malnourished surviving child (M) (n = 386) compared to sibling controls (S) (n = 277).

<p>Boxplot showing weight-for-height, weight-for-age and height-for-age of the ex-malnourished surviving child (M) (n = 386) compared to sibling controls (S) (n = 277).</p

Cox regression exploring clinical and social risk factors for death, by HIV serostatus.

<p>* Adjusted for oedema, age, sex, admission WAZ and admission MUAC.</p

Patient profile at baseline (initial admission), by final outcome.

†<p>Numbers with kwashiorkor plus numbers with severe wasting = 972 rather than 1024: the remaining 52 patients had complicated moderate wasting. These children were treated according to exactly the same protocols as those with SAM and hence are included in the follow-up study.</p

Cox regression exploring main baseline predictors of death.

<p>* Adjusted for age, oedema, and HIV status.</p

Kaplan Meier failure curves, by HIV serostatus.

<p>The tables below <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0096030#pone-0096030-g002" target="_blank">figures 2</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0096030#pone-0096030-g003" target="_blank">3</a> show numbers at risk at the beginning of a particular time period. Deaths are in parentheses. Numbers at risk are not simply those previous at-risk minus deaths. Other outcomes also result in children being removed from further analysis (being ‘censored’). With this denominator change, the y-axis is mortality <i>probability</i> rather than percentage. Whilst our main outcomes focus is on the first year post-discharge, for completeness, data is presented until the last child's follow-up.</p

Plasma ADAMTS13 activity inhibition in <i>P. falciparum</i> malaria.

<p>(A&B) To investigate further the mechanisms responsible for the marked and discrepant increase in plasma VWF∶CB, and the significant reduction in ADAMTS13 activity, we investigated the effects of mixing malaria plasma with normal plasma. Plasma from four different children (□, ●, △, ◆) with SM (each with baseline ADAMTS13 activities of ∼0.4 U/dl) were mixed in various proportions with pooled normal plasma, and ADAMTS13 activity determined. No evidence of an immediate ADAMTS13 inhibitor effect was observed (<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000349#ppat-1000349-g004" target="_blank">Fig 4A</a>). However following incubation at 37°C for 15 min or 30 min (<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000349#ppat-1000349-g004" target="_blank">Fig 4B</a>), significant ADAMTS13 inhibition was observed in malaria plasmas at either 75%∶25% (▲), or 50%∶50% (●), but not in normal control plasma (□). All results represent mean±SEM. (C) To further investigate whether malarial plasma contained an ADAMTS13 inhibitor, individual malaria plasma samples (n = 4) and control plasmas (n = 4) were spiked with recombinant human ADAMTS13. Again, significant inhibition of rADAMTS13 activity (means±SEM) was observed only in malaria plasma (◆) but not in normal plasma (■).</p

Severe <i>Plasmodium falciparum</i> malaria influences plasma VWF antigen level and collagen binding activity.

<p>(A) Plasma VWF∶Ag levels (<i>white bars – left Y axis</i>) were measured by ELISA, and VWF activity by collagen binding activity (VWF∶CB) (<i>grey bars – right Y axis</i>). Each plasma sample was tested in duplicate at three dilutions, and median values for each group are shown. VWF∶Ag and VWF∶CB levels were markedly elevated in patients with cerebral malaria and in children with severe malaria at presentation compared to levels in healthy control children. (B) In a cohort of children with cerebral malaria (CM), the time-course of VWF∶Ag and VWF∶CB levels following admission and commencement of anti-malarial therapy was assessed using follow-up plasma samples collected after 24 and 72 hours respectively. (C) Although both VWF∶Ag and VWF∶CB were increased in all cases of <i>P. falciparum</i> malaria, the relative increase observed in plasma VWF∶CB levels was significantly higher (p<0.05), such that the ratio of CB to Ag was consistently >1 in children with CM (n = 13; ●) or SM (n = 20; ▲) at presentation compared to healthy control subjects (n = 25; □). (<i>Hashed line indicates 1∶1 ratio</i>).</p

Immediate and antecedent causes of death when underlying cause was low birth weight and prematurity complications N9 (N = 404).

Immediate and antecedent causes of death when underlying cause was low birth weight and prematurity complications N9 (N = 404).</p