In conclusion, we demonstrate for the first time, using RNA-seq, profile analysis of periodontitis revealing site-specific local variation in gene expression profiles of periodontitis-affected and healthy tissues obtained from patients diagnosed with periodontitis. Furthermore, we have identified differentially expressed novel genes in gingival tissue of periodontitis. Our findings provide a first step towards a quantitative comprehensive insight into the transcriptome of gingival tissue from patients with periodontitis, to enable identification of possible diagnostic markers of periodontitis as well as potential therapeutic targets. Our findings not only support the hypothesis that UA contributes to the pathogenesis of P. falciparum malaria in African children, but also raises the possibility that the UA level may serve as a useful biomarker for severe disease. In addition, our findings may help to explain those of Sarma et al., who showed that the co-administration of allopurinol and quinine more effectively reduced inflammation than quinine alone in a study of Indian adults with severe P. falciparum malaria. Our data also provide some evidence to support the need for clinical trials to investigate whether allopurinol, which has been safely administered at UA-lowering doses to patients with severe P. falciparum malaria, might be useful as an adjunctive treatment for severe malaria syndromes that kill African children. Whether uricosuric drugs might benefit such patients also merits investigation. This study reports data from a relatively large number of Malian children of all ages who presented with malaria syndromes that were clinically well-defined. To our knowledge, this is the first study to specifically investigate associations between UA and inflammatory cytokines PI-103 during episodes of human malaria. Before making these correlations, we confirmed that the cytokines we measured increase with disease severity, thus implicating them in the pathogenesis of severe malaria in our Malian study population. Previous studies that measured UA levels in patients with malaria tested the hypothesis that UA is an indirect marker of oxidative stress. This is because the formation of UA from hypoxanthine and xanthine generates ROS. Only two previous studies examined the relationship between UA levels and P. falciparum densities in patients with malaria. Bertrand et al. describe a weak correlation in a group of 60 Cameroonian adults with UM. In comparing groups of Nigerian children with asymptomatic parasitemia, UM and severe malaria, Iwalokun et al. showed that the association between UA levels and parasite density gets stronger with disease severity; however, this correlation was significant only in the group of severe cases. Our analysis of 438 Malian children with UM shows a moderate, but highly significant, correlation between UA levels and parasite densities. Our study has several limitations. First, we are unable to identify the cause of elevated UA levels in our patients. During a malaria episode, excess soluble UA may be produced by a variety of processes, including the dissolution of parasite-derived UA precipitates, the conversion of parasite-accumulated hypoxanthine and xanthine to UA by plasma xanthine oxidase, and the hemolysis of both parasitized and non-parasitized RBCs. The levels of UA produced by any of these processes may correlate with parasite density.