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Valérie Biran

Publications and source records attributed to Valérie Biran.

2 recordsLinked to original sources

Investigating cerebral anomalies in preterm infants and associated risk factors with magnetic resonance imaging at term-equivalent age

Background: Being born very or extreme preterm is a major source of cerebral anomalies and neurodevelopmental disorders, whose occurrence depends on many perinatal factors. A better understanding of these factors could be provided by cerebral Magnetic Resonance Imaging (MRI) at term-equivalent age (TEA). Objective: To investigate, through cerebral TEA-MRIs, the relationship between the main perinatal factors, the occurrence of cerebral anomalies, and cerebral volumetry. Methods: We assembled a cohort of preterm babies born before 32 weeks of gestation who underwent a cerebral TEA-MRI. We assessed cerebral anomalies using a radiological scoring system -- the Kidokoro scoring -- and performed cerebral volumetry. We investigated the relationships between 9 clinical factors (birth characteristics, resuscitation treatments{\ldots}), Kidokoro scores, and brain volumes. Results: Among 110 preterms who underwent a cerebral MRI at TEA, only 6% suffered moderate-to-severe brain anomalies. We identified mechanical ventilation as a risk factor for cerebral anomalies (adjusted Odds-Ratio aOR = 4.6, 95% Confidence Interval CI [1.7-12.8]) and prolonged parenteral nutrition as a protective factor for white matter anomalies (aOR = 0.2, 95%CI [0.1-0.8]). Mechanical ventilation (p = 0.01) and being born small for gestational age (p < 0.001) were risk factors for the reduction of cerebral volumes. An increase in brain lesion severity was associated with decreased cerebral volumes (p = 0.016). Conclusion: Our study highlights the importance of treatment-related perinatal factors on the occurrence of cerebral anomalies in very and extreme preterms, and the interest in using both qualitative (Kidokoro scoring) and quantitative (volumetry) MRI-tools.

q-bio.NC↗

Glial activation in white matter following ischemia in the neonatal P7 rat brain

This study examines cell death and proliferation in the white matter after neonatal stroke. In post-natal day 7 injured rat, there was a marked reduction in myelin basic protein (MBP) immunostaining mainly corresponding to numerous pyknotic immature oligodendrocytes and TUNEL-positive astrocytes in the ipsilateral external capsule. In contrast, a substantial restoration of MBP, as indicated by the MBP ratio of left-toright, occurred in the cingulum at 48 (1.27 +- 0.12) and 72 (1.30 +- 0.18, p<0.05) hours of recovery as compared to age-matched controls (1.03 +- 0.14). Ki-67 immunostaining revealed a first peak of newly-generated cells in the dorsolateral hippocampal subventricular zone and cingulum at 72 hours after reperfusion. Double immunofluorescence revealed that most of the Ki-67-positive cells were astrocytes at 48 hours and NG2 pre-oligodendrocytes at 72 hours of recovery. Microglia infiltration occurs over several days in the cingulum and a huge quantity of macrophages reached the subcortical white matter where they engulfed immature oligodendrocytes. The overall results suggest that the persistent activation of microglia involves a chronic component of immunoinflammation, which overwhelms repair processes and contributes to cystic growth in the developing brain.

q-bio.NC↗