Cause of coma of undetermined aetiology in children using 16s rRNA sequencing.
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PROVIDER: PRJEB26897 | ENA |
REPOSITORIES: ENA
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Project description:We used microarrays to characterize the whole blood global gene expression profiles in 98 children with P. falciparum cerebral malaria We associated retinopathy status with host genes and pathways to explore mechanisms of infected red sequestration to the microvasculature in CM
2015-10-30 | GSE72058 | GEO
Project description:We used microarrays to characterize the whole blood global gene expression profiles in 98 children with P. falciparum cerebral malaria We associated retinopathy status with host genes and pathways to explore mechanisms of infected red sequestration to the microvasculature in CM Cross sectional study of chidlren with CM, expression profiling derived from study enrollment whole blood sample RNA isolated from sample stored in Tri-Reagent BD; hybridization with Affymetrix Gene Chip Human Gene 1.0 ST Array.
2015-10-30 | E-GEOD-72058 | biostudies-arrayexpress
Project description:Gene expression patterns were investigated in well-defined genetically cerebral malaria-resistant (CM-R) and cerebral malaria-susceptible (CM-S) mouse strains. cDNA microarrays were used to search for differentially expressed genes in mouse brain. Four mouse strains, known to differ in susceptibility to cerebral malaria upon Plasmodium berghei ANKA infection, were compared: BALB/c and DBA/2 mice are CM-R, while C57BL/6 and CBA/J mice are CM-S.
2005-06-30 | E-MEXP-370 | biostudies-arrayexpress
Project description:PBMCs were obtain from mild malaria and cerebral malaria patient at the onset of P. falciparum infection. Patient recruitment took place in two hospital centers in Senegal Total RNAs from PBMCs of mild and cerebral malaria patients were profiled after hybridization with Agilent SurePrint G3 Human GE 8x60K Microarray to identify blood biomarkers for cerebral malaria phenotype Plasmodium falciparum malaria remains a major health problem in Africa. The mechanisms of pathogenesis leading to the severe form of the disease are not fully understood. Blood transcriptional profiles were investigated in patient with cerebral malaria, noncerebral malaria , and mild malaria by using the microarray technology. We identified a set of 447 genes that was differentially expressed between the three patient groups after a false discovery rate of 10%. Since the cerebral patients displayed a particular transcriptional pattern, we focused our analysis on the differences between cerebral malaria patients and mild malaria patients. We further found 849 genes differentially expressed after a false discovery rate of 10%. We validated our results by using the qPCR method for 5 genes. The enrichment analysis of their functional annotation indicates that genes involved in A, B, C pathways play a role in the occurrence of cerebral malaria. These results provide new insight into the potential effect of the dysregulation of gene expression and specific pathways. Host genetic variation may partly explain such alteration of gene expression. Further studies are required to investigate this in African populations.
2019-10-07 | GSE116306 | GEO
Project description:Cerebral Malaria (CM), the deadliest complication of Plasmodium infection, is a complex and unpredictable disease. Currently, our understanding of the factors that trigger progression of malaria to CM is limited. Here, by infecting experimental CM (ECM) resistant (Balb/c) and ECM susceptible (C57BL/6) mice with ECM causing (ANKA) and non-ECM causing (NK65) Plasmodium berghei (Pb) parasite strains, we revealed that in resistant host, infection by ECM causing parasite develops similar to infection by non-ECM causing parasite in susceptible host in terms of parasite growth in host, disease course and host immune response against parasite. Our comparative gene expression analysis revealed that in Balb/c host, gene expression of Pb ANKA parasite is remarkably different from, the gene expression of Pb ANKA in C57BL/6 but similar to the gene expression of non-ECM causing Pb NK65 in C57BL/6. Thus, host has a critical influence on parasite behavior which ultimately determines the course of malaria disease.
2023-02-21 | GSE215359 | GEO
Project description:Comaprision of P.falciparum clinical isolates showing Uncomplicated disease with that shwoing complicated disease(Cerebral malaria) The experiment was designed to try and identify differences if any, at the genome level between P.falciparum isolates from patients with uncomplicated malaria vs. patients with complicated malaria (Cerebral malaria). The emphasis was to highlight possible amplifications/deletions in different regions of the parasite genome.
2017-01-06 | GSE77165 | GEO
Project description:Cerebral malaria (CM) is one of the most severe complications of malaria infection. There is evidence that repeated parasite exposure promotes resistance against CM, as indicated by the low incidence of CM in adults in malaria-endemic regions. However, the immunological basis of this infection-induced resistance remains poorly understood. Here, a microarray study done utilising the tractable Plasmodium berghei ANKA model of experimental cerebral malaria (ECM), we show that three rounds of infection and drug-cure protects against the development of ECM during a subsequent fourth infection.
2019-02-19 | E-MTAB-5513 | biostudies-arrayexpress
Project description:Micronutrient deficiencies and environmental exposures have been to known to adversely impact brain and nervous system functions in adults and children worldwide. However, few studies have examined the short and long-term impact of these risk factors on neurodevelopmental outcomes in children in low-income countries, where the effects are likely to be more pronounced due to limited resources for monitoring and insufficient regulations. Biological risk factors of relevance include micronutrient deficiencies such as zinc and exposure to heavy metals such as lead and mercury. Studies have suggested an association between neurodevelopmental impairment and micronutrient deficiency as well as exposure to a number of heavy metals and environmental toxins. Moreover, findings also suggest that risk factors for adverse developmental outcomes that are independently significant may have the potential for causing cumulative increases in adverse effects. In Sub-Saharan Africa, severe malaria is a leading risk factor for long-term neurocognitive impairment in children. Zinc deficiency or exposure to heavy metals could influence risk of severe malaria, modify the risk of neurocognitive impairment in children with severe malaria, or independently affect risk of neurocognitive impairment. Untargeted analyses for potential environmental exposures or metabolomic changes in children with cerebral malaria vs. without cognitive impairment or in children with higher vs. lower cognitive scores, could also identify new risk factors for neurodevelopmental impairment in Ugandan children with cerebral malaria.In our completed study in Kampala, we assessed neurologic and developmental impairment in children with cerebral malaria [CM] or severe malarial anemia [SMA], as compared to health community children from the same extended household as the children with CM or SMA. As an extension of this study, we are interested in determining levels of micronutrients such as zinc in the population, and in addition, determining exposure levels of heavy metals (lead, mercury, copper, manganese etc.) in samples collected from children with severe malaria and community controls. The primary hypotheses of this study is that nutrient deficiencies or exposure to heavy metals influence short and long term neurocognitive outcomes in healthy community children and in children with severe malaria, and that children with cerebral malaria have specific metabolomic changes that relate to long-term neurocognitive impairment. The specific aims of our study are:Aim 1: To determine levels of zinc, heavy metals, and biomarkers associated with inflammation in children presenting with different forms of severe malaria (SM) and in healthy community children (CC). The working hypothesis of this aim is that 1) children with SM will have lower zinc levels compared to CC; 2) children with SM will present with higher toxic metal exposure and higher levels of biomarkers associated with inflammation than CC.Aim 2: To investigate how micronutrient deficiency, toxic metal exposure and inflammatory biomarkers affect short and long term neurodevelopmental outcomes and growth in children with severe malaria and community children (CC).The working hypothesis of this aim is that the lower levels of zinc, and presence of toxic metals in high concentrations will independently contribute to worsening neurodevelopmental outcomes and worsening growth over time in children with severe malaria and in community children. An alternate hypothesis is that micronutrient deficiency, toxic metal exposure and inflammatory states may interact with each other and with severe malaria to produce greater neurodevelopmental impairment, i.e., that the contribution is not independent but interactive.Aim 3: To determine whether the CSF metabolome differs according to level of neurodevelopmental impairment in children with cerebral malaria. The working hypothesis of this aim is that neurodevelopmental impairment in children with cerebral malaria is associated with changes in the CSF metabolome.
2017-09-27 | ST000877 | MetabolomicsWorkbench
Project description:By studying differently expressed immune genes with gene expression profiling in immune competent children researchers have been able to distinguish between children with asymptomatic viral infection and those with symptomatic viral infection as well as patients with bacterial infection. In this study we asked if gene expression profiling is feasible as a diagnostic tool in febrile neutropenia. We included children under treatment for a malignancy presenting with febrile neutropenia. Clinical data regarding the infectious episode was prospectively collected and children grouped based on microbiological agent detected into virus, bacteria, co-infection and unknown aetiology. Fourty three episodes had sufficient RNA for RNA-sequencing, 15 with respiratory tract virus, 22 with unknown etiology, 4 with co-infection and 2 with bacteria. No pathogen specific host-innate immune expression profile was seen in the group with virus, bacteria nor unknown aetiology probably due to the low white blood cell account (WBC). In the co-infection group with higher WBC but lower absolute neutrophil count (ANC) compared to the other groups, a downregulated innate response were detected. We conclude that gene expression profiling in children presenting with neutropenic fever is not a feasible diagnostic tool for febrile neutropenia in children with cancer due the low WBC.:
2020-08-26 | GSE152341 | GEO
Project description:Clinically distinguishing acute bacterial meningitis from cerebral malaria, both of which are important causes of acute non-traumatic coma associated with morbidity and mortality among paediatric hospital admissions in malaria endemic areas of Africa, is challenging. Few hospitals have diagnostic capacity for distinguishing the two syndromes resulting in broader antibiotic cover than necessary. A biochemical marker of ABM would facilitate precise clinical diagnosis and management of these infections.
In this study, we used Label-free protein quantification by mass spectrometry to identify components of the CSF protein expression profiles of children with ABM that distinguish from those with CM with a high degree of specificity and sensitivity and that could be developed into point-of-care tests.
James M. Njunge, Ian N. Oyaro, Nelson K. Kibinge, Martin K. Rono, Symon Kariuki, Charles R. Newton, James A. Berkley, Evelyn Gitau
2017-04-24 | MSV000080979 | MassIVE