14 research outputs found

    The ADMA/arginine ratio is acutely elevated in African children with severe malaria.

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    <p>ADMA and arginine concentrations were measured in plasma samples collected at the time of presentation (Day 0) and at follow-up visits 28 days later (Day 28) in children with WHO-defined uncomplicated malaria or severe malaria. Healthy Gambian children served as a reference group. Wilcoxon test was used for pair-wise comparison of admission and day 28 mesurements within individuals (47 paired observations from patients with severe malaria; 65 paired observations from patients with uncomplicated malaria). Mann-Whitney test was used to compare patients with severe malaria (n = 81) versus uncomplicated malaria (n = 75) and to compare patients with uncomplicated malaria versus healthy children (n = 31). Each horizontal line depicts the group median. **** p < 0.0001; ns p > 0.05.</p

    Baseline clinical characteristics of the study population.

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    <p>Values are presented as median [interquartile range]. ADMA: asymmetric dimethylarginine, sVCAM: soluble vascular cell adhesion molecule, PfHRP2: <i>P</i>. <i>falciparum</i> histidine-rich protein 2.</p><p><sup>a</sup> p < 0.001 compared to healthy Gambian children by Mann-Whitney test.</p><p><sup>b</sup> p < 0.001 compared to uncomplicated malaria by Mann-Whitney test.</p><p>Baseline clinical characteristics of the study population.</p

    DDAH regulates NO synthesis via ADMA metabolism.

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    <p>Protein arginine methyltransferases (PRMTs) methylate arginine (Arg) residues on proteins to form asymmetric dimethylarginine (ADMA). Proteolysis releases free ADMA that inhibits nitric oxide synthase (NOS). Dimethylarginine dimethylaminohydrolase (DDAH) metabolizes free ADMA to citrulline (Cit) that can be recycled to arginine. Inactivation of DDAH leads to accumulation of ADMA, inhibition of endothelial NO synthesis, and endothelial dysfunction.</p

    Correlation of ADMA with biomarkers of anemia, hemolysis, parasite biomass, endothelial activity, and tissue perfusion among children with severe malaria.

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    <p>ADMA, Arg, ADMA/Arg, HRP2 and sVCAM were natural log-transformed. Hemoglobin was normally distributed and was not transformed. Lactate was square root-transformed. Haptoglobin could not be transformed to a normally distributed variable. All correlations were calculated using Pearson’s method, except for correlations with haptoglobin which were calculated using Spearman’s method. A plot of each correlation is presented in the supplement (<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005119#ppat.1005119.s005" target="_blank">S3 Fig</a>).</p><p>Correlation of ADMA with biomarkers of anemia, hemolysis, parasite biomass, endothelial activity, and tissue perfusion among children with severe malaria.</p

    ADMA and arginine concentrations in plasma.

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    <p>Values are presented as median [interquartile range]. ADMA: asymmetric dimethylarginine. Day 0 was the day of initial presentation to clinic or hospital.</p><p><sup>a</sup> p < 0.0001 compared to healthy Gambian children by Mann-Whitney test.</p><p><sup>b</sup> p < 0.0001 compared to uncomplicated malaria by Mann-Whitney test.</p><p><sup>c</sup> p < 0.0001 compared to admission by Wilcoxon matched-pairs signed-rank test.</p><p>ADMA and arginine concentrations in plasma.</p

    Multiple linear regression analysis of the relationships between ADMA and arginine and hemoglobin, HRP2, sVCAM, or lactate.

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    <p>ADMA, Arg, HRP2, and sVCAM were natural log-transformed. Lactate was square root-transformed. ADMA and arginine were explanatory variables in four separate linear models predicting hemoglobin, HRP2, sVCAM, or Lactate.</p><p>Multiple linear regression analysis of the relationships between ADMA and arginine and hemoglobin, HRP2, sVCAM, or lactate.</p

    Long (GT)<sub>n</sub> repeats and “L carrier” genotype associate with less severe disease.

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    <p>A) Frequency distribution of the number of [GT]<sub>n</sub> repeats in SM (open bars, n = 282 alleles) and UM cases (black bars, n = 302 alleles). B) Frequency of the “S” (short<27), “M” (medium 27 to 32) and L (long>32) [GT]<sub>n</sub> repeats for SM (open bars) and UM (black bars) cases. C) Frequency of “S” (open bars), “M” (dotted bars) and “L” (black bars) [GT]<sub>n</sub> repeats according to disease entities. Distribution of <i>HMOX1</i> promoter genotypes amongst D) SM (open bars) and UM (black bars) cases, and E) amongst different disease entities. Those labeled in green are “L carriers”, those labeled in red are “non-L carriers”. SM = severe malaria, SRD = severe respiratory distress, CM = cerebral malaria, SA = severe anaemia, SP = severe prostration, UM = uncomplicated malaria.</p

    Association between L allele containing genotype and different disease entities.

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    <p>(SM = severe malaria, all entities, SP = severe prostration, SA = severe anaemia, CM = cerebral malaria, SRD = severe respiratory distress). In the top row, the odds ratio (OR) is shown for the association between L allele carriage and SM/UM, and a risk ratio (RR) is shown for the association between L allele carriage and each of the disease entities versus UM. (CI 95% refers to 95% confidence intervals of the estimates). The second row in italics shows similar results for the corresponding analyses adjusted for ethnicity.</p
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