Relevant bibliographies by topics / Cerebral malaria

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cerebral malaria'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 June 2024

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Journal articles on the topic "Cerebral malaria"

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Mandala, Wilson L., Chisomo L. Msefula, Esther N. Gondwe, James J. Gilchrist, Stephen M. Graham, Paul Pensulo, Grace Mwimaniwa, et al. "Lymphocyte Perturbations in Malawian Children with Severe and Uncomplicated Malaria." Clinical and Vaccine Immunology 23, no. 2 (November 18, 2015): 95–103. http://dx.doi.org/10.1128/cvi.00564-15.

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ABSTRACTLymphocytes are implicated in immunity and pathogenesis of severe malaria. Since lymphocyte subsets vary with age, assessment of their contribution to different etiologies can be difficult. We immunophenotyped peripheral blood from Malawian children presenting with cerebral malaria, severe malarial anemia, and uncomplicated malaria (n= 113) and healthy aparasitemic children (n= 42) in Blantyre, Malawi, and investigated lymphocyte subset counts, activation, and memory status. Children with cerebral malaria were older than those with severe malarial anemia. We found panlymphopenia in children presenting with cerebral malaria (median lymphocyte count, 2,100/μl) and uncomplicated malaria (3,700/μl), which was corrected in convalescence and was absent in severe malarial anemia (5,950/μl). Median percentages of activated CD69+NK (73%) and γδ T (60%) cells were higher in cerebral malaria than in other malaria types. Median ratios of memory to naive CD4+lymphocytes were higher in cerebral malaria than in uncomplicated malaria and low in severe malarial anemia. The polarized lymphocyte subset profiles of different forms of severe malaria are independent of age. In conclusion, among Malawian children cerebral malaria is characterized by lymphocyte activation and increased memory cells, consistent with immune priming. In contrast, there are reduced memory cells and less activation in severe malaria anemia. Further studies are required to understand whether these immunological profiles indicate predisposition of some children to one or another form of severe malaria.
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Beare, Nicholas A. V., Simon J. Glover, and Malcolm Molyneux. "Malarial Retinopathy in Cerebral Malaria." American Journal of Tropical Medicine and Hygiene 80, no. 2 (February 1, 2009): 171. http://dx.doi.org/10.4269/ajtmh.2009.80.171.

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Pikatan, Orlando, Ellen Ferlita Tirtana, Kezia Seraphine, and Wienta Diarsvitri. "BIOMARKERS AND PROGNOSTIC SCORING IN CEREBRAL MALARIA." MNJ (Malang Neurology Journal) 8, no. 2 (July 1, 2022): 140–43. http://dx.doi.org/10.21776/ub.mnj.2022.008.02.13.

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Malaria remains a public health concern and remain the deadliest in infectious disease in the world. Cerebral malaria is a particularly severe complication of this disease and associated with high mortality. This literature review is made up from 19 literatures consisting of journals, and book. The literature review used data base www.pubmed.com, and www.scholar.google.com using “cerebral malaria and biomarker, predictor of cerebral malaria and treatment of severe malaria”. The languages for this journal are English and Indonesian. From the collection of literatures in this literature review, severe consists of cerebral malaria, blackwater fever, acute kidney injury, pulmonary edema, electrolyte disturbance, hematology disturbance, and obstetrics emergency resulting from malaria which is postpartum hemorrhage. Cerebral malaria increases the mortality of the patient, so they have to be diagnosed early and treated precisely. Patients with infection of plasmodium falciparum and GCS<11 must be suspected as cerebral malaria. Biomarker examination such as Soluble ICAM-1, Specific muscle’s protein, Angiopoetin-1 and 2, and Plasma microparticles is the most precise way to detect malarial emergency earlier Coma Acidosis Malaria score is also found to be useful in predicting the prognosis in cerebral malaria. Early diagnosis should be made as early as possible to reduce mortality from malaria and its emergencies.
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Burton, Adrian. "When is cerebral malaria not cerebral malaria?" Lancet Neurology 3, no. 3 (March 2004): 139. http://dx.doi.org/10.1016/s1474-4422(04)00699-4.

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Lawton, Jonathan G., Albert E. Zhou, Drissa Coulibaly, Emily M. Stucke, Antoine Dara, Matthew B. Laurens, Joana C. Silva, Mahamadou A. Thera, and Mark A. Travassos. "272 Differential expression of two Plasmodium falciparum variant surface antigen families in Malian children with cerebral malaria compared to mild malaria." Journal of Clinical and Translational Science 7, s1 (April 2023): 81–82. http://dx.doi.org/10.1017/cts.2023.330.

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OBJECTIVES/GOALS: Recent in vitro evidence suggests that diverse parasite protein families called RIFINs and STEVORs are displayed on the surface of infected red blood cells and may have a role in severe malaria, but they remain sparsely studied in natural infections. We measured the RNA expression of these antigens in Malian children with severe or mild malaria illness. METHODS/STUDY POPULATION: We collected blood samples from Malian children aged six months to five years, including 14 with cerebral malaria, 10 with severe malarial anemia, and demographic-matched controls with mild, uncomplicated malaria. We extracted total RNA from each patient and used a custom capture array to selectively enrich Plasmodium falciparum parasite RNA. We then performed Illumina next-generation RNA sequencing and reconstructed parasite transcriptomes using reference-free de novo assembly. We identified RNA encoding RIFINs and STEVORs using an in-house classifier, then measured the diversity and abundance of gene expression for each infection. Expression diversity was defined as the number of unique variants transcribed. Expression abundance was calculated as transcripts per million (TPM). RESULTS/ANTICIPATED RESULTS: Cerebral malaria cases, but not severe malarial anemia cases, had higher diversity and abundance of RIFIN expression compared to mild infections. Type A RIFINs predominated over Type B RIFINs, and the same two RIFINs were predominantly expressed in all disease phenotypes. We anticipate that predominantly expressed RIFINs share high sequence homology with variants previously shown to bind blood antigens or immune inhibitory receptors. STEVOR expression was also higher in cerebral malaria compared to mild malaria, but STEVOR transcripts were sparse overall. DISCUSSION/SIGNIFICANCE: Elevated RIFIN expression in cerebral malaria over mild malaria supports a role for these antigens in pathogenesis. Severe malarial anemia may progress through a different pathogenic mechanism. Predominantly expressed RIFIN variants may be promising targets for vaccines and therapeutics to protect children against cerebral malaria.
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Burté, Florence, Biobele J. Brown, Adebola E. Orimadegun, Wasiu A. Ajetunmobi, Nathaniel K. Afolabi, Francis Akinkunmi, Olayinka Kowobari, et al. "Circulatory hepcidin is associated with the anti-inflammatory response but not with iron or anemic status in childhood malaria." Blood 121, no. 15 (April 11, 2013): 3016–22. http://dx.doi.org/10.1182/blood-2012-10-461418.

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Aprilen, Nisa, and I. Made Bayu Indratama. "Handling cerebral malaria patient with limited resources: a case report." Jurnal Penyakit Dalam Udayana 5, no. 2 (December 20, 2021): 26–31. http://dx.doi.org/10.36216/jpd.v5i2.149.

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Cerebral malaria is an emergency condition. All patients with Plasmodium falciparum infection followed by neurological symptoms should be treated as cerebral malaria. The pathogenesis of cerebral malaria is caused by the damage of blood vessels endothelium due to parasites sequestration, production of pro-inflammatory cytokines and leakage of blood vessels which can cause brain hypoxia. The proper management is needed, however this become quiet challenging issue in the setting of limited resouces. We report a case of a 35 year old patient presenting with a loss of consciousness accompanied by shivering fever for 5 days. On examination of the peripheral blood smear, the Plasmodium falciparum was found. The patient was later diagnosed as cerebral malaria and treated with anti-malarial drugs. The fifth day of treatment the patient has fully alert. In the next day, the patient was allowed to go home. The management of cerebral malaria is challenging, particularly in the area with limited resources.
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Desruisseaux, Mahalia S., Fabiana S. Machado, Louis M. Weiss, Herbert B. Tanowitz, and Linnie M. Golightly. "Cerebral Malaria." American Journal of Pathology 176, no. 3 (March 2010): 1075–78. http://dx.doi.org/10.2353/ajpath.2010.091090.

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Cartagena, Yuliet, Carolina Monsalve, and María Eugenia Toro. "Malaria cerebral." Acta Neurológica Colombiana 37, no. 1 supl. 1 (March 1, 2021): 148–53. http://dx.doi.org/10.22379/24224022347.

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Mturi, Neema, Crispin O. Musumba, Betty M. Wamola, Bernhards R. Ogutu, and Charles R. J. C. Newton. "Cerebral Malaria." CNS Drugs 17, no. 3 (2003): 153–65. http://dx.doi.org/10.2165/00023210-200317030-00002.

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Dissertations / Theses on the topic "Cerebral malaria"

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MacCormick, I. "Malarial retinopathy and neurovascular injury in paediatric cerebral malaria." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/2049100/.

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Background Diseases of the brain are difficult to study because this organ is relatively inaccessible. Only one part of the central nervous system is available to direct, non-invasive observation – the retina. The concept of the retina as a window to the brain has created much interest in the retina as a source of potential markers of brain disease. Paediatric cerebral malaria is a severe neurological complication of infection with the parasite Plasmodium falciparum, which is responsible for death and disability in a significant number of children in sub-Saharan Africa. As with many neurological diseases, the precise mechanisms by which this infection causes damage to the brain remain unclear, and this hampers efforts to develop effective treatments. It may be that studying the retina in paediatric cerebral malaria could both illuminate pathogenesis specific to this disease, and also provide an illustration of how to approach retinal biomarkers in a new, and potentially more effective way. Methods I approached the aim of developing retinal features as markers of brain disease in paediatric cerebral malaria via several objectives. I made use of an existing clinical study to collect new retinal data from ophthalmoscopic examinations and fundus fluorescein angiograms from patients over three successive malaria seasons in Malawi, and added these to historical data obtained previously at the same site. I devised a new method for grading retinal images. I reviewed the biological plausibility of associations between retina and brain in cerebral malaria, and then considered analytical methods to interpret my retinal data effectively. Finally I estimated associations between retinal features, outcomes, and a radiological measure of brain swelling using combinations of regression models. Results My review of retinal and cerebral histopathology, vascular anatomy and physiology indicated that certain retinal and brain regions may be similarly prone to damage from sequestration as a result of interactions between aberrant rheology and microvascular geometry, such as branching patterns and arteriole to venule ratios. My review of evaluations of analogy and surrogacy suggested that biological similarities between retina and brain could be used to justify statistical evaluation of the amount of information the subject and object of the inference share about a common outcome, as used to assess surrogate end points for clinical trials. This kind of approach is able to address questions about whether a particular retinal feature is effectively equivalent to an analogous disease manifestation in the brain. I report analyses on three overlapping groups of subjects, all of whom had retinopathy positive cerebral malaria: children with admission ophthalmoscopy (n=817), children with admission fluorescein angiography (n=260), and children with admission angiography and MRI of the brain (n=134). Several retinal features are associated with death and longer time to recover consciousness in paediatric cerebral malaria. Broadly speaking, these features appear to reflect two processes: neurovascular sequestration (e.g. orange vessel discolouration and death), and neurovascular leakage (e.g. >5 sites of punctate leak and death). Respective adjusted odds ratios and 95% confidence intervals for these particular associations are: 2.88 (1.64-5.05); and 6.90 (1.52-31.3). Other related processes may also be important, such as ischaemia, which can be extensive. Associations between retina and brain are less clear, in part because of selection bias in the samples. Conclusions Neurovascular leak is important in fatal paediatric cerebral malaria, suggesting that fatal brain swelling may occur primarily as a result of vasogenic oedema. Other processes are also likely to be involved, particularly neurovascular sequestration, which is visible on retinal imaging as orange vessels or intravascular filling defects. Sequestration may plausibly cause leak through direct damage to tight junctions and by increasing transmural pressure secondary to venous congestion. Several types of retinal leakage are seen and some of these may represent re-perfusion rather than acute injury. Future work to investigate temporal changes in retinal signs may find clearer associations with radiological and clinical outcomes. The steps taken to evaluate retinal markers in cerebral malaria illustrate a more rigorous approach to retinal biomarkers in general, which can be applied to other neurological diseases.
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Crawley, Jane Margaret Stewart. "Seizures in childhood cerebral malaria." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396249.

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Dennison, Jeremy M. T. J. "Cytoadhesion, cytokines and cerebral malaria." Thesis, University of Liverpool, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337149.

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Greene, Jennifer A. "Toll-like Receptor Polymorphisms and Cerebral Malaria." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270153850.

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Almelli, Talleh. "Parasite genetic factors implicated in cerebral malaria." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05P605/document.

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Le paludisme à P. falciparum est l’une des causes majeures de mortalité et de morbidité dans le monde. Ce parasite est responsable de plusieurs manifestations cliniques allant du portage asymptomatique et infections non compliquées aigüe au paludisme grave et compliqué, tel que le neuropaludisme. Nous avons émis l’hypothèse que l’expression différentielle des gènes contribue à la variation phénotypique de parasites, entraînant des interactions spécifiques avec l’hôte, qui à son tour déterminent le type de manifestations cliniques du paludisme. L’objectif principal de cette étude était d’identifier les facteurs génétiques de P. falciparum impliqués dans la pathogenèse du neuropaludisme. Ceci a été réalisé par l’analyse complète du transcriptome d’isolats provenant d’enfants camerounais porteurs asymptomatiques (PA) ou atteints d’accès simple (AS) ou de neuropaludisme (NP). Le transcriptome du clone non sélectionnée (3D7) et la lignée sélectionnée (3D7-Lib) a été également analysé. Les résultats ont montré la surexpression de plusieurs gènes chez des isolats provenant d’enfants atteints de neuropaludisme et chez la lignée 3D7-Lib, par rapport à ceux provenant d’enfants asymptomatiques et 3D7, respectivement. L’analyse de l’ontologie de gène indique que les gènes potentiellement impliqués dans la pathogenèse, la cytoadhérence et l’agrégation des érythrocytes sont surreprésentés parmi les gènes surexprimés chez les isolats de CM et 3D7-Lib. Les résultats les plus marquants étaient la surexpression des gènes var (groups A et B) portant les domaines cassettes DC4, DC5, DC8 et DC13 et les gènes avoisinants rif chez les isolats de NP et la lignée 3D7-Lib, par rapport aux isolats de PA et au clone non sélectionné 3D7, respectivement. Le rôle joué par ces gènes dans la virulence parasitaire est lié à la cytoadhérence, c’est-à-dire la capacité de leurs protéines exprimées à interagir entre les érythrocytes parasités et les récepteurs endothéliaux post capillaires. Parmi ces récepteurs, le CD36 et inter cellular adhesion molecule 1 (ICAM-1) ont été les plus couramment utilisés par les isolats. L’étude sur l’implication de ces deux récepteurs, ainsi que celle des ligands PfEMP-1, dans la pathogenèse du neuropaludisme devrait être approfondie poursuivie. Nous avons analysé le phénotype de cytoadhérence et les profils de transcription des variantes de Pfemp-1 des isolats frais provenant des enfants béninois atteints de NP ou AS à l’aide du test d’adhérence statique aux récepteurs CD36, ICAM-1 et CSPG et au moyen de RT-PCR quantitative pour les groupes A, B, var2, var3, DC8 et DC13. Nos résultats montrent que le niveau de cytoadhérence des parasites associés au neuropaludisme au CD36 est significativement plus important que celui des parasites associés à l’accès simple. En outre, nous n’avons pas trouvé de différence significative entre la cytoadhérence des isolats de deux groupes cliniques à ICAM-1 et au CSPG. En outre, les niveaux d’expression des groupes var A, B, var2, var3 et du DC8 et DC13 sont plus élevés chez les isolats associés au neuropaludisme que chez les isolats associés à l’accès simple. Nos résultats montrent également que, chez les parasites provenant de NP le haut niveau de cytoadhérence des parasites au CD36 est corrélé au niveau de l’expression de groupe B de gènes var. En revanche, les profils d’expression des groupes spécifiques du gène var et le phénotype de cytoadhérence aux récepteurs ICAM-1 et CSPG n’étaient pas corrélés. Nos résultats suggèrent un rôle important du récepteur CD36 et des protéines codées par les variantes de PfEMP-1 codées par le groupe B dans la pathogenèse du neuropaludisme
Plasmodium falciparum infection is a major cause of mortality and morbidity worldwide. This parasite is involved in several clinical manifestations, ranging from asymptomatic carriage and acute uncomplicated to severe and complicated malaria, including cerebral malaria. We hypothesized that differential gene expression contributes to phenotypic variation of parasites leading to specific interaction with the host which induces several clinical categories of malaria. The principal aim of this study was to identify parasite genetic factors implicated in the pathogenesis of cerebral malaria. We investigated the whole transcriptome of parasites isolated from Cameroonian children with asymptomatic (AM), uncomplicated (UM) and cerebral malaria (CM). We also investigated the transcriptome of 3D7 clone and the selected 3D7-Lib line. Our results revealed the up-regulation of several genes in CM isolates and 3D7-Lib line compared to AM isolates and 3D7 clone respectively. Gene ontology analysis indicates an over-representation of genes implicated in pathogenesis, cytoadherence, and erythrocyte aggregation among up-regulated genes in CM and 3D7-Lib. The most remarkable outcomes were the up-regulation of UPS A and B var genes containing architectural Domains Cassettes DC4, DC5, DC8, and DC13 and their neighboring rif genes in isolates from CM and 3D7-Lib line, compared with isolates from AM and the unselected 3D7 line, respectively. The involvement of these genes in parasite virulence rises from the ability of their encoded proteins to mediate cytoadherence of infected erythrocytes to post-capillary endothelial receptors. Of these receptors, CD36 and Inter Cellular Adhesion Molecule-1 (ICAM-1) were found as the most commonly used by the isolates. The implication of these two receptors, as well as that of PfEMP-1 ligands in the pathogenesis of CM needs to be more elucidated. We examined the adhesive phenotype and the transcription patterns of Pfemp-1 variants of fresh isolates from Beninese children with CM or UM malaria by static binding assay to CD36, ICAM-1 and CSPG and RT-qPCR for groups A, B, var2, var3, DC8, and DC13. Our findings showed that isolates from CM patients bind more to CD36 than those from UM cases. No differences were observed in binding levels to ICAM-1 or CSPG between these two groups. Furthermore, CM isolates transcribed groups A, B, var2, var3, DC8 and DC13 of var genes at higher levels than UM isolates. Interestingly, the high transcription levels of group B in CM parasites correlated with their higher level of binding to CD36. In contrary, the expression profiles of a specific var group and the binding phenotype of isolates to ICAM-1 and to CSPG were not correlated. Our findings support the implication of CD36 along with PfEMP-1 variants encoded by group B in cerebral malaria pathogenesis
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Weiser, Silvia. "In vitro studies on the pathogenesis of cerebral malaria." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28140.

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Malaria is caused by infection with the protozoan Plasmodium. About 40% of the world’s population is at risk, nearly all of them living in the least developed countries. While 300-500 million cases are reported per year, about 2 million people die annually. Most of the fatal cases develop severe malaria, which is a complication of Plasmodium fulciparum infection. Symptoms can include multi-organ dysfunction, anaemia, lung complications and cerebral malaria (CM). Although the pathogenesis is controversial, there are two main theories to explain the aetiology of CM: sequestration of parasitised red blood cells (pRBC) and leukocytes in the vasculature, and an over-reaction of the immune system. In the latter case, enhanced production of deleterious immune effectors such as cytokines is involved. Experimental models of CM (in vitro and in vivo) have been developed because clinical studies are hampered by ethical constraints and post-mortem human tissue is hard to obtain. CBA or C57BL/6 mice infected with Plasmodium berghei ANKA (PbA) succumb to murine CM and show progressive behavioural, histopathological and immunological changes. In contrast, Plasmodium berghei K173 (PbK)-infected C57BL/6 mice die due to anaemia and hyperparasitaemia, but without neurological symptoms. Although it is important to study the disease in the whole animal, in vitro studies are helpful to elucidate mechanisms at the cellular level. It is known that various cell types contribute to the pathogenesis of CM. In particular, endothelial cells lining the cerebral microvasculature are involved in the development of CM. They form part of the blood-brain barrier (BBB) which tightly regulates the traffic of substances and cells into the brain parenchyma to protect cerebral cells and to maintain the intemeuronal milieu. The permeability of the BBB is increased early after infection (day 3-4 p.i.) in the murine experimental model of CM. This might lead to an influx of deleterious substances into the cerebral parenchyma, causing the neurological symptoms observed. Changes at the microvascular endothelium are thought to contribute to the leakage of the BBB. In response to various stimulants ECs increase the expression of cellular adhesion molecules (CAM) on their surface. Cells such as leucocytes (in murine CM) and pRBCs (in human CM) adhere to the vessels, recruiting an immune response to the area.
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Newton, Charles R. J. C. "Intracranial hypertension in Kenyan children with cerebral malaria." Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27054.

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Cerebral malaria is a common encephalopathy in African children, but the cause of death and neurological sequelae are unknown. This dissertation examines the hypothesis that raised intracranial pressure (ICP) is a determinant of poor outcome in Kenyan children with cerebral malaria. The opening cerebrospinal fluid pressure was raised in all 26 children in whom it was measured on admission and 92% of 35 children in whom it was measured after admission. Brain stem signs, particularly an abnormal respiratory pattern, absent pupillary responses and a lack of spontaneous eye movement were associated with a death. In 33 children who died with cerebral malaria, at least 18-42% had clinical features of transtentorial herniation, according to the criteria used. Intracranial pressure monitoring was performed in 18 children with severe CM, of whom 14 had computerised tomography (CT) and in 10 the basal cranial arteries were monitored with transcranial Doppler (TCD) sonography. Three children with severe intracranial hypertension (maximum ICP > 60 mmHg and minimum cerebral perfusion pressure (CPP) < 40 mmHg) had a poor outcome despite aggressive therapy with mannitol. One child with a maximum ICP of 151 mmHg died with the signs of uncal and medullary stages of herniation. In the other 2 children, middle cerebral artery velocity and vascular resistance monitored with TCD sonography changed with ICP and CPP. Both of these children had diffuse brain swelling associated with generalised hypodensity on their acute CT scans. These children survived° with cerebral atrophy on their convalescent scans and severe neurological deficits. In the 8 children with intermediate intracranial hypertension (maximum ICP 20-60 mmHg and CPP < 50 mmHg) mannitol was effective in controlling the intracranial hypertension. TCD was not reliable in detecting changes in ICP or CPP. Two of these children had acute brain swelling, but the tomographic density was normal and the swelling had resolved when the repeat scans were performed 12-24 days later. All the children with intermediate intracranial hypertension survived without major neurological sequelae. In the remaining 7 children who had ICP monitoring, the maximum ICP was <20 mmHg and mannitol was not administered. None of the CT scans showed brain swelling and the children survived without severe sequelae. In a further 9 children with severe malaria (6 with CM) the agonal stages were monitored with TCD. Three children with CM had sonographic features of progressive intracranial hypertension associated with signs of herniation, whilst the other children (including 3 with CM) did not have these sonographic features, although one had evidence of brainstem compromise before dying. Thus raised ICP is a feature of CM in Kenyan children. Severe intracranial hypertension is associated with a poor outcome and could be responsible for at least a third of the children dying from CM. Mannitol reduces the ICP, but does not prevent nor control severe intracranial hypertension.
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Bakmiwewa, Supun Madushani. "The Astrocyte: a Crossroads in Cerebral Malaria Pathogenesis." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14952.

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Cerebral malaria (CM) is a severe complication of malaria, and involves the central nervous system (CNS). Despite the significant negative impact of CM, its pathogenesis is not fully understood. Two theories, namely cerebral hypoxia and cytokine expression, are considered to be involved in the process. The present study investigated the potential interaction of these two theories in driving the development of CM. Astrocytes can be a major determinant of the outcome of CNS diseases, and we hypothesised that astrocytes, by responding to the pathways involved in the two theories, would drive the development of CM. The cytokines interferon-gamma (IFN-γ) and lymphotoxin-alpha (LT-α) are essential for the development of experimental CM in a murine model. The chemokine C-X-C motif ligand 10 (CXCL10) also is implicated in this process. Both Malawian paediatric and mouse CM brain samples showed increased cytokine expression and astrocyte activation. Furthermore, by the use of Ifnγ-/- mice, it was shown that IFN-γ was involved in this CM-associated astrocyte activation. Cultured human primary astrocytes were directly activated by IFN-γ and LT-α to produce synergistic levels of CXCL10. This finding provides a potential mechanism by which astrocytes could be involved in the pathogenesis of CM, and sheds light on the possible role of LT-α in CM. Hypoxia had an effect on astrocytes, but their response to cytokines was not altered by hypoxia. However, oxygen-glucose deprivation resulted in a decline in cytokine-induced CXCL10 release by cultured astrocytes. Decreased production of CXCL10 has the potential to translate into less blood brain barrier damage. Thus, the mechanisms underlying these two theories do interact at the astrocyte level, but astrocytes show both protective and pathological features as a result of this interaction. The present thesis shows that it is unlikely that the two mechanisms act together to reinforce the astrocytes’ pathological effects to cause CM.
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Shaw, Tovah. "Defining the immunological basis of cerebral pathology during murine experimental cerebral malaria and understanding the basis of infection induced resistance." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/defining-the-immunological-basis-of-cerebral-pathology-during-murine-experimental-cerebral-malaria-and-understanding-the-basis-of-infection-induced-resistance(cef82ee4-61f7-4f27-afb3-e0ffd1906bd7).html.

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Malaria affects 200 million people annually, resulting in 584,000 - 1,238,000 deaths. The majority of these deaths occur in children, less than 5 years of age, in sub-Saharan Africa and are due to cerebral malaria (CM), a neuropathology induced primarily by the species Plasmodium (P.) falciparum. The pathogenesis of CM remains poorly understood and the mechanisms involved in acquired protection against the syndrome in malaria-endemic regions are undefined. Utilising the well characterised P. berghei ANKA experimental infection model of cerebral malaria (ECM), results presented in this thesis show that the development of ECM is associated with the accumulation and arrest of pathogenic CD8+ T cells within the perivascular spaces of the brain. Accumulation of activated CD8+ T cells, without arrest, was observed in the perivascular spaces of the brains of mice infected with the non-ECM causing P. berghei NK65 strain. These data show that the behaviour of intracerebral CD8+ T cells specifies their pathogenic function during malaria infection. The development of ECM was associated with extensive disruption to the BBB, which developed in the absence of extensive CD8+ T cell-dependent endothelial cell apoptosis. We modified the ECM model, establishing an infection-drug cure strategy, to investigate the immunological basis of parasite exposure-induced resistance to ECM development. Three rounds of infection-drug cure promoted resistance to ECM, which was associated with reduced intracerebral expression of genes involved in defence response, regulation of apoptosis, chemotaxis, CTL activity, antigen processing and presentation and cell adhesion, compared with ECM susceptible mice. Additionally, CD8+ T cell activation was suppressed in exposure-induced resistant mice and was associated with the antibody dependent expansion of a splenic plasmacytoid DC population, with a regulatory phenotype. The infection-induced protection against ECM was critically dependent upon secreted antibody production. A long standing problem in studying the immune response to malaria infection has been the inability to track parasite-specific CD4+ T cell responses. To address this, we generated and validated new transgenic P. berghei parasites expressing the model antigen, ovalbumin (OVA), either in the parasite cytoplasm or on the parasitophorous vacuole membrane (PVM). We found that cellular location and expression level of the antigen influence the induction and magnitude of parasite-specific T-cell responses. These parasites thus provide knowledge on the factors that influence the recognition of parasite antigens by the immune system and represent useful tools to study the development and function of antigen-specific T-cell responses during malaria infection. The results in this thesis improve our understanding of the events that lead to the development of CM, and the host immune responses that develop following parasite exposure to protect against it. The results should contribute towards the rational development of adjunctive therapies and effective vaccines for human CM.
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Campino, Susana Gomes. "Genetic analysis of murine malaria /." Umeå : Univ, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-124.

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Books on the topic "Cerebral malaria"

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Kiwirra, Khalid El Amin. Cerebral malaria: Pharmacological approaches. Genève: Atelier de reproduction de la Section de Physique, 1997.

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World Health Organization. Division of Control of tropical Diseases. Packaged treatment for first line care in Cerebral Malaria and Meningitis. Malawi: World Health Organization, 1997.

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Bronzan, Rachel. Peripheral parasite density and its relationship to severity of disease in pediatric cerebral malaria. [New Haven, Conn: s.n.], 1995.

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Standards for adjudicating claims presented by veterans suffering from hepatitis C, cerebral malaria, and Persian Gulf illnesses: Hearing before the Subcommittee on Benefits of the Committee on Veterans' Affairs, House of Representatives, One Hundred Fifth Congress, second session, July 16, 1998. Washington: U.S. G.P.O., 1999.

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I, Rapoport Stanley, Fondation IPSEN pour la recherche thérapeutique., and Colloque médecine et recherche (5th : 1989 : Lille, France), eds. Imaging, cerebral topography, and Alzheimer's disease. Berlin: Springer-Verlag, 1990.

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Thakur, Kiran. Malaria. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0163.

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Malaria persists despite efforts for global eradication and vaccine development, and continues to prove lethal in endemic regions. The neurological manifestations of malaria are often devastating, with a high mortality rate and significant morbidity in survivors. A major life threatening complication of malaria infection is cerebral malaria (CM), most commonly occurring in children in sub-Saharan Africa and adults in Southeast Asia. There should be a high suspicion for CM in patients who present in coma residing in or having recently traveled to malaria endemic regions. Other neurological manifestations posing significant morbidity include postmalaria neurological syndrome and side effects due to antimalarial medications. Discussions in this chapter are focused around the neurobiology of malaria infection, and the host- and pathogen-related factors that contribute to neurological manifestations of the mosquito-borne illness.
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Whitty, Christopher J. M. Diagnosis and management of malaria in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0292.

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Falciparum malaria is the commonest life-threatening imported tropical infection. The most important critical care intervention is rapid high-dose antimalarial treatment with artesunate, or if that is not available quinine. The common complications of malaria are different in children and adults. Cerebral malaria may occur in both, for which there is no specific therapy. Renal failure and acute lung injury are much more common in adults, and may occur late in the course of the disease, even after parasites have cleared. In children acidosis, anaemia and Gram-negative sepsis are more common. Renal and respiratory support may be needed in adults. Malaria alone seldom causes shock and if patients are shocked, co-existing Gram-negative sepsis should be considered. In children there is evidence that bolus hydration increases mortality. Most patients make a full recovery even after prolonged periods of unconsciousness.
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US GOVERNMENT. Standards for adjudicating claims presented by veterans suffering from hepatitis C, cerebral malaria, and Persian Gulf illnesses: Hearing before the Subcommittee ... Congress, second session, July 16, 1998. For sale by the U.S. G.P.O., Supt. of Docs., Congressional Sales Office, 1999.

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Rapoport, Stanley I., Didier Leys, and Henri Petit. Imaging, Cerebral Topography and Alzheimer's Disease. Springer London, Limited, 2011.

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Rapoport, Stanley I., Didier Leys, and Henri Petit. Imaging, Cerebral Topography and Alzheimer's Disease. Springer London, Limited, 2013.

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Book chapters on the topic "Cerebral malaria"

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Abbasi, Adeel, Francis DeRoos, José Artur Paiva, J. M. Pereira, Brian G. Harbrecht, Donald P. Levine, Patricia D. Brown, et al. "Cerebral Malaria." In Encyclopedia of Intensive Care Medicine, 535–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_811.

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Wilairatana, Polrat, and Srivicha Krudsood. "Cerebral Malaria." In International Neurology, 285–89. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch80.

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Wilairatana, Polrat, Srivicha Krudsood, and Noppadon Tangpukdee. "Cerebral malaria." In International Neurology, 268–72. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch71.

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Park, Gregory S., and Chandy C. John. "Cerebral Malaria." In Neuroinflammation and Neurodegeneration, 405–28. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1071-7_19.

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Grau, Georges Emile Raymond, and Samuel Crocodile Wassmer. "Pathogenetic Immune Responses in Cerebral Malaria." In Malaria, 67–80. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45210-4_4.

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Kampondeni, S. D., and M. J. Potchen. "MRI Neuroimaging in Pediatric Cerebral Malaria." In Encyclopedia of Malaria, 1–14. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-8757-9_84-1.

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Davis, Timothy M. E., Moses Laman, and Laurens Manning. "Cerebral Malaria: Pathophysiology of Clinical Features." In Encyclopedia of Malaria, 1–10. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8757-9_99-1.

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Aikawa, Masamichi. "The Pathology of Cerebral Malaria." In Host Response to International Parasitic Zoonoses, 53–68. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68281-3_6.

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Bienvenu, Anne-Lise, and Stephane Picot. "Cerebral Malaria: Protection by Erythropoietin." In Methods in Molecular Biology, 315–24. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-308-4_19.

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White, Valerie Ann, Valentina Barrera, and Ian James Callum MacCormick. "Ocular Pathology of Cerebral Malaria." In Methods in Molecular Biology, 749–63. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2189-9_55.

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Conference papers on the topic "Cerebral malaria"

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Fedosov, Dmitry A., Bruce Caswell, and George Em Karniadakis. "Multiscale Modeling of Blood Flow in Cerebral Malaria." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13012.

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Healthy red blood cells (RBCs) have relatively soft membranes that allow them to pass through narrow capillaries of the diameter as small as 3 μm. Recent experiments [1] showed that malaria-parasitized RBCs are characterized by a considerable stiffening of their membranes compared to healthy RBCs. This results in an increased blood flow resistance in the capillary bed, and may lead to an obstruction of small capillaries and significant blood-flow reduction. In addition, malaria-infected cells are able to adhere to each other and endothelium in arterioles and venules leading to more severe blood-flow reduction or blockage. Blood flow in cerebral malaria is extremely complex due to the mentioned effects, and requires multiscale modeling of RBCs and adhesive interactions. We developed a coarse-grained RBC model which is able to accurately reproduce RBCs mechanics and dynamics for different malaria stages: ring-trophozoite-schizont from the earliest to the latest. RBC adhesion is simulated based on the stochastic bond formation/dissociation model, which is able to capture complex adhesive dynamics.
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Desai, K., A. Agarwal, and J. E. Sevransky. "A Rare Case of Cerebral Malaria with Neurologic Recovery." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2948.

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Bilodeau, J., B. Ward, N. Brewster, and A. Schwartz. "Catastrophic Cerebral Malaria as a Cause for Refractory Distributive Shock." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1759.

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Zhao, Xiaojin, Amine Bermak, and Farid Boussaid. "A low cost CMOS polarimetric ophthalmoscope scheme for cerebral malaria diagnostics." In 2011 IEEE/IFIP 19th International Conference on VLSI and System-on-Chip (VLSI-SoC). IEEE, 2011. http://dx.doi.org/10.1109/vlsisoc.2011.6081598.

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Trindade Maranhao Costa, Fabio, and JoÃo Conrado Khouri Dos Santos. "Effect of Hyperbaric Oxygen Therapy on thrombosis in murine cerebral malaria." In XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil: Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-38055.

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Glick, J., F. Canaday, D. Roberts, S. Palka, A. Falsey, and M. A. Nead. "An Exceptional Instance: Severe Malaria With Cerebral Complications in Western New York." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5630.

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Liu, Xun, David A. Rice, and Bahram Khoobehi. "Spectral reflectance of the ocular fundus as a diagnostic marker for cerebral malaria." In SPIE BiOS, edited by Robert J. Nordstrom and Gerard L. Coté. SPIE, 2012. http://dx.doi.org/10.1117/12.905763.

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Muschta, I., and C. Hornberger. "Bilateral deafness in a case of a 15-year old girl caused by cerebral malaria." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728398.

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Anuar, Adzly, Farid Mahamud, Juniza Md Saad, and Kesavan Rana Singam. "Design of a Wearable Walking Aid Based on Anthropometric Measurement of Cerebral Palsy Children in Malaysia." In 2018 3rd International Conference on Control, Robotics and Cybernetics (CRC). IEEE, 2018. http://dx.doi.org/10.1109/crc.2018.00020.

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Hamzah, Fatimahwati, and Saiful Hasley Ramli. "A Systematic Review of Assistive Technology Devices to Promote Independent Living in Children with Cerebral Palsy." In Proceedings of the 2nd International Conference on Design Industries & Creative Culture, DESIGN DECODED 2021, 24-25 August 2021, Kedah, Malaysia. EAI, 2022. http://dx.doi.org/10.4108/eai.24-8-2021.2315270.

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Reports on the topic "Cerebral malaria"

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Oakley, Miranda S. Molecular Factors and Biological Pathways Associated with Malaria Fever and the Pathogenesis of Cerebral Malaria. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ad1014029.

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