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Brain Infection (brain + infection)
Selected AbstractsDelta-9-Tetrahydrocannabinol (THC), the Major Psychoactive Component of Marijuana, Exacerbates Brain Infection by AcanthamoebaTHE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 2001FRANCINE MARCIANO-CABRAL [source] Absence of pestivirus antigen in brains with white matter damageDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2006Olaf Dammann We previously suggested that antenatal pestivirus infection might play a role in the pathogenesis of perinatal brain white matter damage (WMD) in preterm infants. We have now examined 22 brains from stillborns and deceased newborns (both preterm and term) for the presence of bovine virus diarrhoea virus (BVDV) antigen. The brains of five females and five males with WMD (median gestational age 36.5wks), and nine female and three male controls (median gestational age 36.5wks) were used in the study. No BVDV antigen was detected in any of the 22 brains. We conclude that brain infection with BVDV is unlikely to play a role in WMD pathogenesis among preterm or term newborns. Further research is needed to test the hypothesis that intrauterine exposure to pestivirus antigen elicits a fetal inflammatory response which then contributes to WMD. [source] New molecular markers of early and progressive CJD brain infectionJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2004Zhi Yun Lu Abstract Transmissible spongiform encephalopathies (TSEs), including human Creutzfeldt,Jakob disease (CJD), are caused by a related group of infectious agents that can be transmitted to many mammalian species. Because the infectious component of TSE agents has not been identified, we examined myeloid cell linked inflammatory pathways to find if they were activated early in CJD infection. We here identify a specific set of transcripts in CJD infected mouse brains that define early and later stages of progressive disease. Serum amyloid A3 and L-selectin mRNAs were elevated as early as 20 days after intracerebral inoculation. Transcripts of myeloid cell recruitment factors such as MIP-1,, MIP-1,, and MCP1, as well as IL1, and TNF, were upregulated >10 fold between 30 and 40 days, well before prion protein (PrP) abnormalities that begin only after 80 days. At later stages of symptomatic neurodegenerative disease (100,110 days), a selected set of transcripts rose by as much as 100 fold. In contrast, normal brain inoculated controls showed no similar sequential changes. In sum, rapid and simple PCR tests defined progressive stages of CJD brain infection. These markers may also facilitate early diagnosis of CJD in accessible peripheral tissues such as spleen and blood. Because some TSE strains can differentially target particular cell types such as microglia, several of these molecular changes may also distinguish specific agent strains. The many host responses to the CJD agent challenge the assumption that the immune system does not recognize TSE infections because these agents are composed only of the host's own PrP. © 2004 Wiley-Liss, Inc. [source] | ||||||||||