White Matter Cell Death (white_matter + cell_death)

Distribution by Scientific Domains


Selected Abstracts


Effect of maternal antibiotic treatment on fetal periventricular white matter cell death in a rabbit intrauterine infection model

ACTA PAEDIATRICA, Issue 1 2003
T Debillon
Aim: To evaluate the effects of maternal antibiotic treatment on fetal brain cell death in a rabbit intrauterine infection model. Methods: After Escherichia coli uterine-horn inoculation in 22 pregnant rabbits, followed at various times by ceftriaxone and caesarean section, cell death in white matter (histology and fragmented DNA staining) from fetuses killed at extraction was compared across groups using the Mantel-Haenszel test and Fisher's exact test for small numbers. Results: White matter cell death was consistently present at 48 h, with ceftriaxone initiation at 24 h (group 1), detectable at 84 but not 60 h, with ceftriaxone initiation at 12 h, and significantly reduced at 84 h with ceftriaxone initiation at 6 h (60% vs 100% in group 1, p < 0.001, Fisher's exact test). Conclusion: Early maternal antibiotic therapy delays white matter cell death in rabbit fetuses exposed to intrauterine infection. This may provide a window for preventing white matter damage. [source]


Gestational Hypoxia Induces White Matter Damage in Neonatal Rats: A New Model of Periventricular Leukomalacia

BRAIN PATHOLOGY, Issue 1 2004
Olivier Baud
In the premature infant, periventricular leukomalacia, usually related to hypoxic-ischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sparague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2 -90% N2) from embryonic day 5(E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from p0 to P14 than in controls. Specific white matter cysts wear detected between p0 and p7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period. [source]


Effect of maternal antibiotic treatment on fetal periventricular white matter cell death in a rabbit intrauterine infection model

ACTA PAEDIATRICA, Issue 1 2003
T Debillon
Aim: To evaluate the effects of maternal antibiotic treatment on fetal brain cell death in a rabbit intrauterine infection model. Methods: After Escherichia coli uterine-horn inoculation in 22 pregnant rabbits, followed at various times by ceftriaxone and caesarean section, cell death in white matter (histology and fragmented DNA staining) from fetuses killed at extraction was compared across groups using the Mantel-Haenszel test and Fisher's exact test for small numbers. Results: White matter cell death was consistently present at 48 h, with ceftriaxone initiation at 24 h (group 1), detectable at 84 but not 60 h, with ceftriaxone initiation at 12 h, and significantly reduced at 84 h with ceftriaxone initiation at 6 h (60% vs 100% in group 1, p < 0.001, Fisher's exact test). Conclusion: Early maternal antibiotic therapy delays white matter cell death in rabbit fetuses exposed to intrauterine infection. This may provide a window for preventing white matter damage. [source]