Cerebral malaria: why experimental murine models are required to understand the pathogenesis of disease.
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Endothelial-Leukocyte Interaction in Severe Malaria: Beyond the BrainEndothelin-1 and its role in the pathogenesis of infectious diseasesVascular dysfunction as a target for adjuvant therapy in cerebral malariaExperimental Cerebral Malaria Spreads along the Rostral Migratory StreamThe machinery underlying malaria parasite virulence is conserved between rodent and human malaria parasitesA rapid murine coma and behavior scale for quantitative assessment of murine cerebral malariaExperimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrierReal-time imaging reveals the dynamics of leukocyte behaviour during experimental cerebral malaria pathogenesisThe exported protein PbCP1 localises to cleft-like structures in the rodent malaria parasite Plasmodium bergheiNitric oxide synthase dysfunction contributes to impaired cerebroarteriolar reactivity in experimental cerebral malariaStatins decrease neuroinflammation and prevent cognitive impairment after cerebral malariaNeuroimmunological blood brain barrier opening in experimental cerebral malariaThe role of animal models for research on severe malariaPharmacologic inhibition of CXCL10 in combination with anti-malarial therapy eliminates mortality associated with murine model of cerebral malariaAngiotensin II Moderately Decreases Plasmodium Infection and Experimental Cerebral Malaria in MiceInhaled nitric oxide reduces endothelial activation and parasite accumulation in the brain, and enhances survival in experimental cerebral malariaSequestration and Tissue Accumulation of Human Malaria Parasites: Can We Learn Anything from Rodent Models of Malaria?Inactivation of a Plasmodium apicoplast protein attenuates formation of liver merozoitesRegulation of immunopathogenesis during Plasmodium and Toxoplasma infections: more parallels than distinctions?Toxoplasma gondii upregulates interleukin-12 to prevent Plasmodium berghei-induced experimental cerebral malaria.Nitrone-based therapeutics for neurodegenerative diseases: their use alone or in combination with lanthionines.Molecular correlates of experimental cerebral malaria detectable in whole bloodA novel role for von Willebrand factor in the pathogenesis of experimental cerebral malariaPlasmodium falciparum histidine-rich protein II causes vascular leakage and exacerbates experimental cerebral malaria in mice.Host Resistance to Plasmodium-Induced Acute Immune Pathology Is Regulated by Interleukin-10 Receptor Signaling.Chitinase 3-like 1 is induced by Plasmodium falciparum malaria and predicts outcome of cerebral malaria and severe malarial anaemia in a case-control study of African childrenRole of the aryl hydrocarbon receptor in the immune response profile and development of pathology during Plasmodium berghei Anka infectionEfficacy of different nitric oxide-based strategies in preventing experimental cerebral malaria by Plasmodium berghei ANKA.An N-ethyl-N-nitrosourea (ENU)-induced dominant negative mutation in the JAK3 kinase protects against cerebral malariaLoss of Toll-like receptor 7 alters cytokine production and protects against experimental cerebral malariaNatural transmission of Plasmodium berghei exacerbates chronic tuberculosis in an experimental co-infection modelThe subcellular location of ovalbumin in Plasmodium berghei blood stages influences the magnitude of T-cell responses.Damage to the blood-brain barrier during experimental cerebral malaria results from synergistic effects of CD8+ T cells with different specificitiesNitric oxide protection against murine cerebral malaria is associated with improved cerebral microcirculatory physiology.Endothelial cells potentiate interferon-γ production in a novel tripartite culture model of human cerebral malaria.Dietary restriction protects against experimental cerebral malaria via leptin modulation and T-cell mTORC1 suppressionExogenous nitric oxide decreases brain vascular inflammation, leakage and venular resistance during Plasmodium berghei ANKA infection in mice.Differential microRNA expression in experimental cerebral and noncerebral malaria.Phosphatidylinositol 3-Kinase γ is required for the development of experimental cerebral malaria.Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
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Cerebral malaria: why experimental murine models are required to understand the pathogenesis of disease.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 23 December 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@en
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@nl
type
label
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@en
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@nl
prefLabel
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@en
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@nl
P2093
P921
P1433
P1476
Cerebral malaria: why experime ...... d the pathogenesis of disease.
@en
P2093
J Brian de Souza
Julius C R Hafalla
Kevin N Couper
P304
P356
10.1017/S0031182009991715
P577
2009-12-23T00:00:00Z