1. Lipids of chick retina during ontogenesis --;2. Protein synthesis by differentiating neuro-blasts and glioblasts in cell culture: a model system for analysis of genetic neurologic disease --;3. Morphologic maturation of the brain: a quantitative study --;4. Factors contributing to abnormal neuronal development in the cerebral cortex of the human infant --;5. Assessment and significance of behavioural states --;6. Sleep behavior: genetic regulation --;7. Developmental plasticity in the visual cortex --;8. Language representation and brain development --;9. Zinc and the developing nervous system: toxic effects of zinc on the central nervous system of the preweanling rabbit --;10. Morphologic and biochemical effects of hormones on the developing nervous system in mammals --;11. Effects of drugs, narcotics and toxins on the chemical maturation of the infant brain --;12. Toxic effects of elevated oxygen tension on brain maturation --;13. Nerve growth factor --;14. Viral infections and brain development --;15. Infectious and immunologic diseases affecting the developing nervous system --;16. Biochemical aspects of the maturation of serotoninergic neurons in the rat brain --;17. The development of central catecholamine neuron systems: some implications for disease --;18. Developmental retardation in rat brain after perinatal seizures --;19. Pathophysiologic basis for the selective vulnerability of the immature rat brain TO seizures --;20. Post-natal seizures clinical effects --;21. Specific postnatal threats to brain development: dendritic changes --;22. Metabolic aspects of cerebral anoxia-asphyxia in the fetus and newborn --;23. Postnatal maturation of the local cerebral circulation --;24. Methods for promoting functional recovery following brain damage.
SUMMARY OR ABSTRACT
Text of Note
In order to supplement Dr. Johnson's review we wish to make two points: I) not all grossly similar lesions should be considered t. o be due to the same etiology, even if experimentally documented, and 2) relatively few infections (syphilis, toxoplasmosis, cytomegalovirus, herpesvirus and rubella) and no immunologic disorders (except for kernicterus due to hyperbilirubinemia) are known to affect the developing human nervous system. Admittedly, since most human malformations are of unproven cause, these two points are not mutually exclusive. Rather, the challenge remains to show that any of the experimental models relates to any of the human diseases. In particular, the porencephaly-hydranencephaly spectrum could be due to ischemia in the watershed distribution of one or more branches of the internal carotid ar teries; and aqueductal stenosis could be due to secondary blockage by blood clots or debris related to hemorrhage or necrosis in the germinal matrix or periventricular white matter, lesions most likely due to hypoxia-acidosis in premature infant, who die most often of the concomitant respiratory distress syndrome. REFERENCES Altshuler. G. : Toxoplasmosis as a cause of hydranencephaly. Am. l. Dis. Child. 125: 251-252 (1973). Beer. A.E. and Billingham. R.E. : Immunobiology of mammalian reproduction. Adv. Immunol. 14: 1-84 (1971). Berenberg. W. and Nakervis. G. : Long-term follow-up of cytomegalic inclusion disease of in fancy. Pediatrics 46: 403-410 (1970). Boniuk. M. and Zimmerman. L.E. : Ocular pathology in the rubella syndrome. Arch. Ophthalmo!. 77: 455-473 (1967).