Relevant bibliographies by topics / Pulmonary and 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 'Pulmonary and cerebral malaria'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Pulmonary and cerebral malaria"

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Milner, Danny, Rachel Factor, Rich Whitten, Richard A. Carr, Steve Kamiza, Geraldine Pinkus, Malcolm Molyneux, and Terrie Taylor. "Pulmonary pathology in pediatric cerebral malaria." Human Pathology 44, no. 12 (December 2013): 2719–26. http://dx.doi.org/10.1016/j.humpath.2013.07.018.

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Torre, Sabrina, Sebastien P. Faucher, Nassima Fodil, Silayuv E. Bongfen, Joanne Berghout, Jeremy A. Schwartzentruber, Jacek Majewski, et al. "THEMIS Is Required for Pathogenesis of Cerebral Malaria and Protection against Pulmonary Tuberculosis." Infection and Immunity 83, no. 2 (December 1, 2014): 759–68. http://dx.doi.org/10.1128/iai.02586-14.

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We identify anN-ethyl-N-nitrosourea (ENU)-induced I23N mutation in the THEMIS protein that causes protection against experimental cerebral malaria (ECM) caused by infection withPlasmodium bergheiANKA.ThemisI23Nhomozygous mice show reduced CD4+and CD8+T lymphocyte numbers. ECM resistance inP. bergheiANKA-infectedThemisI23Nmice is associated with decreased cerebral cellular infiltration, retention of blood-brain barrier integrity, and reduced proinflammatory cytokine production. THEMISI23Nprotein expression is absent from mutant mice, concurrent with the decreased THEMISI23Nstability observedin vitro. Biochemical studiesin vitroand functional complementationin vivoinThemisI23N/+:Lck−/+doubly heterozygous mice demonstrate that functional coupling of THEMIS to LCK tyrosine kinase is required for ECM pathogenesis. Damping of proinflammatory responses inThemisI23Nmice causes susceptibility to pulmonary tuberculosis. Thus, THEMIS is required for the development and ultimately the function of proinflammatory T cells.ThemisI23Nmice can be used to study the newly discovered association ofTHEMIS(6p22.33) with inflammatory bowel disease and multiple sclerosis.
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Punnath, Kishore, Kiran K. Dayanand, Valleesha N. Chandrashekar, Rajeshwara N. Achur, Srinivas B. Kakkilaya, Susanta K. Ghosh, Suchetha N. Kumari, and D. Channe Gowda. "Association between Inflammatory Cytokine Levels and Thrombocytopenia during Plasmodium falciparum and P. vivax Infections in South-Western Coastal Region of India." Malaria Research and Treatment 2019 (April 11, 2019): 1–10. http://dx.doi.org/10.1155/2019/4296523.

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Background. Thrombocytopenia is a most commonly observed complication during malaria infections. Inflammatory cytokines such as IL-1, IL-6, and IL-10 have been documented in malaria induced thrombocytopaenia. This study was aimed to understand the possible relationship between inflammatory cytokines across varying degrees of thrombocytopenia during P. vivax, P. falciparum, and mixed infections. Methods. A hospital-based cross sectional study was conducted at District Wenlock Hospital in Mangaluru, a city situated along the south-western coastal region of Arabian Sea in India. In this study, blood samples from 627 malaria patients were analyzed for infected parasite species, clinical conditions, platelet levels, and key cytokines that are produced in response to infection; samples from 176 uninfected healthy individuals were used as controls. Results. The results of our study showed a high prevalence of malarial thrombocytopenia (platelets <150 ×103/μl) in this endemic settings. About 62.7% patients had mild-to-moderate levels of thrombocytopenia and 16% patients had severe thrombocytopenia (platelets <50 × 103/μl). Upon comparison of cytokines across varying degrees of thrombocytopenia, irrespective of infecting species, the levels of TNF-α and IL-10 were significantly higher during thrombocytopenia, whereas IL-6 levels were considerably lower in severe thrombocytopenia patients suffering from P. vivax or P. falciparum infections. The severe clinical complications observed in patients with malarial thrombocytopenia included severe anemia (17.5%), acute renal failure (12.7%), jaundice (27.0%), metabolic acidosis (36.5%), spontaneous bleeding (3.2%), hypoglycemia (25.4%), hyperparasitemia (4.8%), acute respiratory distress syndrome (1.6%), pulmonary edema (19.0%), and cerebral malaria (1.6%) in various combinations. Conclusion. Overall, the results of our study suggest that inflammatory cytokines influence the transformation of mild forms of thrombocytopenia into severe forms during malarial infections. Further studies are needed to understand the association of inflammatory cytokine responses with severe malaria complications and thrombocytopenia.
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Mathur, Arvind, Mohit Kackar, Indu Thanvi, and Harish Agarwal. "STUDY OF CLINICAL FEATURES AND EPIDEMIOLOGY OF COMPLICATED VIVAX MALARIA." International Journal of Research -GRANTHAALAYAH 7, no. 9 (September 30, 2019): 47–51. http://dx.doi.org/10.29121/granthaalayah.v7.i9.2019.556.

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Severe and complicated malaria is defined by the World Health Organization Malaria Action Programme in June 19851 as the presence of one or more of the following conditions in a slide confirmed diagnosed case of malaria cerebral malaria, severe anemia, renal failure, pulmonary edema or adult respiratory distress syndrome, hypoglycemia, circulatory collapse or shock, spontaneous bleeding, repeated generalized convulsions, acidemia or acidosis, macroscopic hemoglobinuria, impairment of consciousness less marked than unarousable coma,, hyperparasitemia, jaundice, hyperpyrexia, and the presence of complicating or associated infections. However, severe anemia and thrombocytopenia that causes bleeding diatesis is produced by hemolysis, reduced cell deformity of parasitized and non-parasitized erythrocytes, increased splenic clearance, reduction of platelet survival, decreased platelet production, and increased splenic uptake of platelets. Though these changes can be produced by P. vivax and P. falciparum infection yet the complicated malaria has commonly been associated with P. falciparum infections.
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Sianti, Eka, and Jose Meky Mandei. "Confusions and dilemma around hepatic dysfunction associated falciparum malaria: A case report and brief review of the literature." Paediatrica Indonesiana 49, no. 4 (August 31, 2009): 244. http://dx.doi.org/10.14238/pi49.4.2009.244-8.

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Malaria remains a big burden in East Indonesia. Severe malaria assaults children in endemic area and leads toenormous morbidities and mortalities.According to the World Health Organization's criteria,recognition of one or more of the following clinicalfeatures should raise the suspicion of severe malariai.e, cerebral malaria (unrousable coma), severe anemia(hemoglobin <5 g/dl), renal failure (creatinine serum> 3 mg/dl), pulmonary edema or adult respiratory distresssyndrome (ARDS), hypoglycemia (glucose < 40 mg/dl),circulatory collapse or shock, disseminated intravascularcoagulation (DIC), repeated generalized convulsions,acidosis (pH < 7 .25), macroscopic hemoglobinuria,hyperparasitaemia ( > 5% of the erythrocytes infested byparasites), or jaundice (bilirubin> 3 mg/dl).l-3Jaundice in malaria due to hepatic dysfunction isa classical case, nevertheless, there are some confusionsand dilemmas in managing it.1 We report a case withjaundice due to hepatic dysfunction and hemolysisassociated falciparum malaria that we treated inGeneral Hospital of Fakfak, West Papua, and providea brief literature review on the matter.
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Hansen, Diana S., Krystal J. Evans, Marthe C. D'Ombrain, Nicholas J. Bernard, Adrienne C. Sexton, Lynn Buckingham, Anthony A. Scalzo, and Louis Schofield. "The Natural Killer Complex Regulates Severe Malarial Pathogenesis and Influences Acquired Immune Responses to Plasmodium berghei ANKA." Infection and Immunity 73, no. 4 (April 2005): 2288–97. http://dx.doi.org/10.1128/iai.73.4.2288-2297.2005.

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ABSTRACT The natural killer complex (NKC) is a genetic region of highly linked genes encoding several receptors involved in the control of NK cell function. The NKC is highly polymorphic, and allelic variability of various NKC loci has been demonstrated in inbred mice. Making use of BALB.B6-Cmv1r congenic mice, in which the NKC from disease-susceptible C57BL/6 mice has been introduced into the disease-resistant BALB/c background, we show here that during murine malaria infection, the NKC regulates a range of pathophysiological syndromes such as cerebral malaria, pulmonary edema, and severe anemia, which contribute to morbidity and mortality in human malaria. Parasitemia levels were not affected by the NKC genotype, indicating that control of malarial fatalities by the NKC cells does not operate through effects on parasite growth rate. Parasite-specific antibody responses and the proinflammatory gene transcription profile, as well as the TH1/TH2 balance, also appeared to be influenced by NKC genotype, providing evidence that this region, known to control innate immune responses via NK and/or NK T-cell activation, can also significantly regulate acquired immunity to infection. To date, NKC-encoded innate system receptors have been shown mainly to regulate viral infections. Our data provide evidence for critical NKC involvement in the broad immunological responses to a protozoan parasite.
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IOANNIDIS, LISA J., CATHERINE Q. NIE, and DIANA S. HANSEN. "The role of chemokines in severe malaria: more than meets the eye." Parasitology 141, no. 5 (December 13, 2013): 602–13. http://dx.doi.org/10.1017/s0031182013001984.

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SUMMARYPlasmodium falciparummalaria is responsible for over 250 million clinical cases every year worldwide. Severe malaria cases might present with a range of disease syndromes including acute respiratory distress, metabolic acidosis, hypoglycaemia, renal failure, anaemia, pulmonary oedema, cerebral malaria (CM) and placental malaria (PM) in pregnant women. Two main determinants of severe malaria have been identified: sequestration of parasitized red blood cells and strong pro-inflammatory responses. Increasing evidence from human studies and malaria infection animal models revealed the presence of host leucocytes at the site of parasite sequestration in brain blood vessels as well as placental tissue in complicated malaria cases. These observations suggested that apart from secreting cytokines, leucocytes might also contribute to disease by migrating to the site of parasite sequestration thereby exacerbating organ-specific inflammation. This evidence attracted substantial interest in identifying trafficking pathways by which inflammatory leucocytes are recruited to target organs during severe malaria syndromes. Chemo-attractant cytokines or chemokines are the key regulators of leucocyte trafficking and their potential contribution to disease has recently received considerable attention. This review summarizes the main findings to date, investigating the role of chemokines in severe malaria and the implication of these responses for the induction of pathogenesis and immunity to infection.
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Jha, Sanjeev, and Mohd Khateebullah Ansari. "Leptospirosis presenting as acute meningoencephalitis." Journal of Infection in Developing Countries 4, no. 03 (January 25, 2010): 179–82. http://dx.doi.org/10.3855/jidc.646.

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Leptospirosis in humans is a common zoonotic disease. It is often under-diagnosed, especially when associated with neurological features, resulting in significant morbidity and mortality. This subgroup of patients with neurological manifestations is often empirically treated for cerebral malaria, dengue fever, tuberculous meningitis, hepatic encephalopathy, viral encephalitis, etc. Hence it is important to be aware of uncommon manifestations of this disease. We report one such patient, which highlights the importance of considering leptospirosis as the diagnostic possibility with hepato-renal, pulmonary and nervous system involvement, particularly where diagnostic supports and resources are limited.
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RYG-CORNEJO, VICTORIA, ANN LY, and DIANA S. HANSEN. "Immunological processes underlying the slow acquisition of humoral immunity to malaria." Parasitology 143, no. 2 (January 8, 2016): 199–207. http://dx.doi.org/10.1017/s0031182015001705.

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SUMMARYMalaria is one of the most serious infectious diseases with ~250 million clinical cases annually. Most cases of severe disease are caused by Plasmodium falciparum. The blood stage of Plasmodium parasite is entirely responsible for malaria-associated pathology. Disease syndromes range from fever to more severe complications, including respiratory distress, metabolic acidosis, renal failure, pulmonary oedema and cerebral malaria. The most susceptible population to severe malaria is children under the age of 5, with low levels of immunity. It is only after many years of repeated exposure, that individuals living in endemic areas develop clinical immunity. This form of protection does not result in sterilizing immunity but prevents clinical episodes by substantially reducing parasite burden. Naturally acquired immunity predominantly targets blood-stage parasites and it is known to require antibody responses. A large body of epidemiological evidence suggests that antibodies to Plasmodium antigens are inefficiently generated and rapidly lost in the absence of ongoing exposure, which suggests a defect in the development of B cell immunological memory. This review summarizes the main findings to date contributing to our understanding on cellular processes underlying the slow acquisition of humoral immunity to malaria. Some of the key outstanding questions in the field are discussed.
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El-Assaad, Fatima, Julie Wheway, Andrew John Mitchell, Jinning Lou, Nicholas Henry Hunt, Valery Combes, and Georges Emile Raymond Grau. "Cytoadherence of Plasmodium berghei-Infected Red Blood Cells to Murine Brain and Lung Microvascular Endothelial CellsIn Vitro." Infection and Immunity 81, no. 11 (August 12, 2013): 3984–91. http://dx.doi.org/10.1128/iai.00428-13.

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ABSTRACTSequestration of infected red blood cells (iRBC) within the cerebral and pulmonary microvasculature is a hallmark of human cerebral malaria (hCM). The interaction between iRBC and the endothelium in hCM has been studied extensively and is linked to the severity of malaria. Experimental CM (eCM) caused byPlasmodium bergheiANKA reproduces most features of hCM, although the sequestration of RBC infected byP. bergheiANKA (PbA-iRBC) has not been completely delineated. The role of PbA-iRBC sequestration in the severity of eCM is not well characterized. Using static and flow cytoadherence assays, we provide the first directin vitroevidence for the binding of PbA-iRBC to murine brain and lung microvascular endothelial cells (MVEC). We found that basal PbA-iRBC cytoadherence to MVECs was significantly higher than that of normal red blood cells (NRBC) and of RBC infected withP. bergheiK173 (PbK173-iRBC), a strain that causes noncerebral malaria (NCM). MVEC prestimulation with tumor necrosis factor (TNF) failed to promote any further significant increase in mixed-stage iRBC adherence. Interestingly, enrichment of the blood for mature parasites significantly increased PbA-iRBC binding to the MVECs prestimulated with TNF, while blockade of VCAM-1 reduced this adhesion. Our study provides evidence for the firm, flow-resistant binding to endothelial cells of iRBC from strain ANKA-infected mice, which develop CM, and for less binding of iRBC from strain K173-infected mice, which develop NCM. An understanding ofP. bergheicytoadherence may help elucidate the importance of sequestration in the development of CM and aid the development of antibinding therapies to help reduce the burden of this syndrome.
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Dissertations / Theses on the topic "Pulmonary and cerebral malaria"

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Palomo, Jennifer. "Etude des réponses immunitaires de l'hôte dans la pathogenèse d'infections : modèles murins de mucoviscidose et malaria." Thesis, Orléans, 2013. http://www.theses.fr/2013ORLE2063/document.

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La mucoviscidose est une pathologie pulmonaire causée par un dysfonctionnement du canal CFTR et caractérisée par un mucus visqueux, une susceptibilité accrue aux infections chroniques et une inflammation excessive. Une première partie de ma thèse a eu pour objectif d’étudier les mécanismes inflammatoires impliqués dans le développement de la pathologie. Nous avons plus particulièrement analysé le rôle de l’IL-1β et de l’IL-17 dans la réponse à l’infection par Pseudomonas aeruginosa, dans le modèle murin ΔF508 de mucoviscidose. La seconde partie de ma thèse a porté sur l’étude de la malaria pulmonaire et cérébrale, une complication létale de l’infection à P. falciparum. Nous avons mis en évidence l’importance de trois voies d’activation des lymphocytes T CD8+ cytotoxiques dans le développement de la neuropathologie induite par Plasmodium berghei ANKA chez la souris : la protéine PKC-θ, la sous-unité β2 du récepteur à l’IL-12 et le récepteur des IFN de type I, mais qui ne semblent pas impliquées dans l’inflammation pulmonaire associée
Cystic fibrosis is a pulmonary pathology, caused by the CFTR channel dysfunction, and characterized by high mucus viscosity, increased sensitivity to chronic infections and excessive inflammation. The aim of my thesis was first to study the inflammatory mechanisms involved in this lung pathology. Indeed, we analyzed the role of IL-1β and IL-17 in response to Pseudomonas aeruginosa infection, in the ΔF508 mouse model of cystic fibrosis. In the second part of my thesis, I studied pulmonary and cerebral malaria, a lethal complication of P. falciparum infection. We showed the importance of three pathways implicated in cytotoxic CD8+ T lymphocytes activation during the Plasmodium berghei ANKA-induced neuropathology development in mice: PKC-θ protein, β2 subunit of IL-12 receptor and type I IFN receptor, which did not seem essential for the associated lung inflammation
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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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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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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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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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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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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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Ball, Elisabeth Ann. "Uncovering the role of IFNAR1 in Experimental Cerebral malaria." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2013. http://hdl.handle.net/10362/11964.

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Dissertation presented the Ph.D degree in Biology
Cerebral malaria is a severe and fatal form of clinical Plasmodium falciparum infection, resulting in brain injury from a damaging cascade of vascular, inflammatory and immunological host responses. However progression to cerebral malaria can be modified by host genetic factors. This thesis work extensively reveals the role of Interferon type I receptor (IFNAR1) in the development of Experimental cerebral malaria, through the use of the mouse model Ifnar1-/-. We found Ifnar1-/- mice protected from Experimental cerebral malaria upon infection with Plasmodium berghei ANKA-GFP, compared with susceptible wild-type C57BL/6 mice. Ifnar1-/- mice showed diminished blood brain barrier breakage, despite parasite accumulation in the periphery and accumulation of immune cells within the brain tissue during infection.(...)
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Books on the topic "Pulmonary and 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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Kuncevskaya, Irina. Regenerative therapy of cerebral disorders in patients with chronic obstructive pulmonary disease at the stage of sanatorium rehabilitation. ru: INFRA-M Academic Publishing LLC., 2020. http://dx.doi.org/10.12737/1045706.

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The monograph first presents modern concepts of comprehensive rehabilitation therapy of cerebral disorders in patients with chronic obstructive pulmonary disease at the stage of sanatorium rehabilitation. Using these data in the practice of medicine will improve the effectiveness of diagnostics, therapy and rehabilitation of cerebral disorders in patients with chronic obstructive pulmonary disease and to provide the students, residents, and graduate students of medical schools, neurologists, physiatrists, pulmonologists, internists, rehabilitation specialists, relevant professional competence. Designed for doctors, students and teachers of medical colleges and universities, and will also be useful for the system of training and retraining of medical workers.
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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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Bradley, Elizabeth M. Infectious diseases: U.S. response. New York: Nova Science Publishers, 2012.

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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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Kanjia, Megha. Cerebral Palsy. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0062.

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Cerebral palsy (CP) is a neurologic disorder characterized by spasticity and is strongly associated with prematurity and low birth weight. Patients with CP often have other related comorbidities including but not limited to gastroesophageal reflux disease, chronic aspiration, immobility, pulmonary conditions, epilepsy, and contractures. These conditions contribute to the need for repeated surgical procedures and also affect the patient’s anesthetic management. Special consideration should be placed on temperature homeostasis, patient positioning, procedural analgesia, and pulmonary support. This chapter defines CP and discusses its clinical manifestations, anesthetic considerations in a pediatric patient requiring surgery, and anesthetic plans for patients with CP and existing comorbidities.
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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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Book chapters on the topic "Pulmonary and cerebral malaria"

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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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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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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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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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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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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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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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Grau, Georges Emile Raymond, and Elham Hosseini-Beheshti. "Extracellular Vesicles and Cerebral Malaria." In Subcellular Biochemistry, 501–8. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67171-6_20.

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Conference papers on the topic "Pulmonary and 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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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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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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Fatania, G., M. Patel, JE Jackson, and CL Shovlin. "P175 Burden of cerebral infarcts identified by screening cerebral mri scans in patients with pulmonary arteriovenous malformations." In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.317.

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Batista, Camila, Helena D’Anunciação De Oliveira, Ana Maria Garcia-Darze, Maiara Lima, Érica Amorim, Adriano Silva, Hugo Caire Castro-Faria-Neto, and Tatiana Maron-Gutierrez. "The effect of combined therapy using rosuvastatin and dihydroarteminin in a pulmonary malaria mouse model." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4290.

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Ferreira, Marcos, Lucas Antunes, Carina Gonçalves, Uyla Garcia, Mônica Almeida, Cláudio Ribeiro, Patricia Martins, and Flávia Gomes. "Phenotypic and functional characterization of innate immunity cells in the establishment of murine pulmonary malaria." In International Symposium on Immunobiological. Instituto de Tecnologia em Imunobiológicos, 2021. http://dx.doi.org/10.35259/isi.2021_46638.

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Lynch, Jennifer M., E. M. Buckley, P. Schwab, B. D. Hanna, D. J. Licht, and A. G. Yodh. "Cerebral Hemodynamic Effects of Hyperoxia Linked to Severity of Pediatric Pulmonary Hypertension." In Biomedical Optics. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/biomed.2012.jm3a.24.

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Reports on the topic "Pulmonary and cerebral malaria"

1

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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