ReviewFrontiers in cellular and infection microbiology2014
Fatal cerebral malaria: a venous efflux problem.
Review in Frontiers in cellular and infection microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- CD8+ T cells target cerebrovasculature in children with cerebral malaria.The Journal of clinical investigation · 2020Trial
- Advancing Understanding of Cerebrovascular Hemodynamic Perturbations in Pediatric Cerebral Malaria Using a Modified Critical Closing Pressure Evaluation- A Prospective, Observational Study.Neurocritical care · 2025Observational
- Small tissue chips with big opportunities for space medicine.Life sciences in space research · 2022Article
- Brain endothelial STING1 activation byProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Impact of Plasmodium vivax malaria on executive and cognitive functions in elderlies in the Brazilian Amazon.Scientific reports · 2022Article
- Interaction Between the Complement System and Infectious Agents - A Potential Mechanistic Link to Neurodegeneration and Dementia.Frontiers in cellular neuroscience · 2021Review
- Brain Endothelium: The "Innate Immunity Response Hypothesis" in Cerebral Malaria Pathogenesis.Frontiers in immunology · 2018Review
- Microvasculature-on-a-chip for the long-term study of endothelial barrier dysfunction and microvascular obstruction in disease.Nature biomedical engineering · 2018Article
- Cerebral malaria induces electrophysiological and neurochemical impairment in mice retinal tissue: possible effect on glutathione and glutamatergic system.Malaria journal · 2017Article
- Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments.Infection and immunity · 2017Article
- Pathophysiological Mechanisms in Gaseous Therapies for Severe Malaria.Infection and immunity · 2016Review
- Characteristics and critical function of CD8+ T cells in the Toxoplasma-infected brain.Seminars in immunopathology · 2015Review
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most Plasmodium falciparum-infected children with cerebral malaria (CM) die from respiratory arrest, but the underlying pathology is unclear. Here we present a model in which the ultimate cause of death from CM is severe intracranial hypertension. Dynamic imaging of mice infected with P. berghei ANKA, an accepted model for experimental CM, revealed that leukocyte adhesion impairs the venous blood flow by reducing the functional lumen of postcapillary venules (PCV). The resulting increase in intracranial pressure (ICP) exacerbates cerebral edema formation, a hallmark of both murine and pediatric CM. We propose that two entirely different pathogenetic mechanisms-cytoadherence of P. falciparum-infected erythrocytes in pediatric CM and leukocyte arrest in murine CM-result in the same pathological outcome: a severe increase in ICP leading to brainstem herniation and death from respiratory arrest. The intracranial hypertension (IH) model unifies previous hypotheses, applies to human and experimental CM alike, eliminates the need to explain any selective recognition mechanism Plasmodium might use to target multiple sensitive sites in the brain, and explains how an intravascular parasite can cause so much neuronal dysfunction.
Indexed as
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.