Because the correlation coefficient for HPLC-B and BCF is very similar to that found for HPLC-B and laboratory TSB, BC could be used not only as a screening device but also as a reliable substitute of TSB determination. At higher levels of TSB, in which phototherapy and/or exchange transfusion might be considered, BC performed slightly better than the laboratory. The accuracy and precision of the TcB measurement in this study was observed to be comparable to the standard of care laboratory test.

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Continuous generation of new neurons has been demonstrated in the adult mammalian brain, and this process was shown to be stimulated by various pathologic conditions, including cerebral ischemia. Because brain oxygen deprivation is particularly frequent in neonates and represents the primary event of asphyxia, we analyzed long-term consequences of transient hypoxia in the newborn rat. Within 24 h after birth, animals were exposed to 100% N 2 for 20 min at 36°C, and temporal changes in the vulnerable CA1 hippocampus were monitored. Cell density measurements revealed delayed cell death in the pyramidal cell layer reflecting apoptosis, as shown by characteristic nuclear morphology and expression levels of Bcl-2, Bax, and caspase-3. Neuronal loss was confirmed by reduced density of neuron-specific enolase (NSE)-labeled cells, and peaked by 1 wk post insult, to reach 27% of total cells. A gradual recovery then occurred, and no significant difference in cell density could be detected between controls and hypoxic rats at postnatal d 21. Repeated injections of bromodeoxyuridine (50 mg/kg) showed that newly divided cells expressing neuronal markers increased by 225% in the germinative subventricular zone, and they tended to migrate along the posterior periventricle toward the hippocampus. Therefore, transient hypoxia in the newborn rat triggered apoptosis in the CA1 hippocampus followed by increased neurogenesis and apparent anatomical recovery, suggesting that the developing brain may have a high capacity for self-repair. (Pediatr Res 55: 561-567, 2004) Abbreviations BrdU, bromodeoxyuridine CO, cytochrome oxidase DAPI, 4,6-diamidino-2-phenylindole DG, dentate gyrus NSE, neuron-specific enolase SVZ, subventricular zone Transient reduction of oxygen supply to the brain is a common feature of the perinatal period, and remains a major cause of neurologic damage (1-3). Depending on the characteristics of the initial insult, consequences may vary from restricted neuronal loss to extensive brain infarction, reflecting the participation of an apoptotic-necrotic continuum (4 -7). In this respect, hypoxic insults have been associated with delayed selective neuronal apoptosis that involves the active participation of specific gene products (8 -12).The brain response to oxygen deprivation appears as a balance between the activation of neurodestructive components and endogenous protective mechanisms (5, 10). Among the various adaptative responses of the brain to severe injury, it has been recently reported that new neurons can be generated through the proliferation of progenitor cells, and thus might help to repair the damaged CNS (13,14). Several studies have documented that experimental ischemia in the adult brain can trigger neurogenesis as a compensatory mechanism to neural cell death (15)(16)(17)(18)(19). Indeed, it is now clearly established that continuous generation of new neurons occurs in the adult mammalian brain (20,21). Newborn cells originate from specific germinative zones, namely the SVZ surrounding the lateral ventr...

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