Cerebral lesions in mice infected with Plasmodium berghei are the result of an immunopathological reaction.

No abstract is available for this paper.

• Publication year

  1989

• Venue

  Transactions of the Royal Society of Tropical Medicine and Hygiene

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/0035-9203(89)90615-9PMID 2696153
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Tumor necrosis factor (cachectin) as an essential mediator in murine cerebral malaria.

  1987cited by this paper
• L3T4+ T lymphocytes play a major role in the pathogenesis of murine cerebral malaria.

  1986cited by this paper
• Control of cachectin (tumor necrosis factor) synthesis: mechanisms of endotoxin resistance.

  1986cited by this paper

• Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

  2021cites this paper
• Persistent cognitive and motor deficits after successful antimalarial treatment in murine cerebral malaria.

  2010cites this paper
• Experimental models of cerebral malaria.

  2005cites this paper
• Increased c-fos expression in the brain during experimental murine cerebral malaria: possible association with neurologic complications.

  1997cites this paper
• Effects of endotoxin and dexamethasone on cerebral malaria in mice

  1995cites this paper
• Pathology of fatal and resolving Plasmodium berghei cerebral malaria in mice

  1992cites this paper