When and Why Do Brain Cells Die?

[1]  M. Cuénod,et al.  Murine brain macrophages induce NMDA receptor mediated neurotoxicity in vitro by secreting glutamate , 1991, Neuroscience Letters.

[2]  M. Raff,et al.  Social controls on cell survival and cell death , 1992, Nature.

[3]  G. Lundborg,et al.  Insulin-like growth factor I (IGF-I) stimulates regeneration of the rat sciatic nerve , 1989, Brain Research.

[4]  J. Rice,et al.  The influence of immaturity on hypoxic‐ischemic brain damage in the rat , 1981, Annals of neurology.

[5]  P. Gluckman,et al.  Accumulation of calcitonin-gene related peptide-like immunoreactivity after hypoxic-ischaemic brain injury in the infant rat. , 1992, Brain research. Molecular brain research.

[6]  J. Beckman The double-edged role of nitric oxide in brain function and superoxide-mediated injury. , 1991, Journal of developmental physiology.

[7]  M. Moskowitz,et al.  Growth factor expression after stroke. , 1990, Stroke.

[8]  P. Gluckman,et al.  Is the Cure Worse than the Disease? Caveats in the Move from Laboratory to Clinic , 1992, Developmental medicine and child neurology.

[9]  A. Gunn,et al.  Outcome after ischemia in the developing sheep brain: An electroencephalographic and histological study , 1992, Annals of neurology.

[10]  S. Rothman The neurotoxicity of excitatory amino acids is produced by passive chloride influx , 1985, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[11]  M. Thordstein,et al.  Cerebral Tolerance of Hypoxia in Growth-Retarded and Appropriately Grown Newborn Guinea Pigs , 1988, Pediatric Research.

[12]  D. Choi Cerebral hypoxia: some new approaches and unanswered questions , 1990, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[13]  P. Gluckman,et al.  A role for IGF-1 in the rescue of CNS neurons following hypoxic-ischemic injury. , 1992, Biochemical and biophysical research communications.

[14]  P. Andiné,et al.  The excitatory amino acid antagonist kynurenic acid administered after hypoxic-ischemia in neonatal rats offers neuroprotection , 1988, Neuroscience Letters.

[15]  F J Schuier,et al.  Experimental Brain Infarcts in Cats: II. Ischemic Brain Edema , 1980, Stroke.

[16]  C. Cotman,et al.  Brain injury causes a time-dependent increase in neuronotrophic activity at the lesion site. , 1982, Science.

[17]  J. Schwaber,et al.  Selective and nonselective stimulation of central cholinergic and dopaminergic development in vitro by nerve growth factor, basic fibroblast growth factor, epidermal growth factor, insulin and the insulin-like growth factors I and II , 1990, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[18]  Y. Shiga,et al.  Neutrophil as a mediator of ischemic edema formation in the brain , 1991, Neuroscience Letters.

[19]  E. Kohmura,et al.  Basic Fibroblast Growth Factor Prevents Thalamic Degeneration after Cortical Infarction , 1991, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[20]  R. Myers,et al.  Effect of Hypoxia on Fetal Brain , 1984 .

[21]  R. Vannucci Experimental Biology of Cerebral Hypoxia-Ischemia: Relation to Perinatal Brain Damage , 1990, Pediatric Research.

[22]  A. Gunn,et al.  Effects of hypoxia-ischemia and seizures on neuronal and glial-like c-fos protein levels in the infant rat , 1990, Brain Research.

[23]  D. Giulian Ameboid microglia as effectors of inflammation in the central nervous system , 1987, Journal of neuroscience research.

[24]  A. Gunn,et al.  Hypoxia-ischemia induces transforming growth factor beta 1 mRNA in the infant rat brain. , 1992, Brain research. Molecular brain research.

[25]  B. Siesjö,et al.  Calcium Fluxes, Calcium Antagonists, and Calcium-Related Pathology in Brain Ischemia, Hypoglycemia, and Spreading Depression: A Unifying Hypothesis , 1989, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[26]  R. Myers,et al.  Delayed Neurologic Deterioration Following Anoxia: Brain Mitochondrial and Metabolic Correlates , 1989, Journal of neurochemistry.

[27]  K. Nicolaides,et al.  Prenatal asphyxia, hyperlacticaemia, hypoglycaemia, and erythroblastosis in growth retarded fetuses. , 1987, British medical journal.

[28]  C. Robertson,et al.  Inhibition of mononuclear phagocytes reduces ischemic injury in the spinal cord , 1990, Annals of neurology.

[29]  K. Takakura,et al.  Amelioration of delayed neuronal death in the hippocampus by nerve growth factor , 1991, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[30]  M. Kowada,et al.  Cerebral ischemia. III. Vascular changes. , 1968, The American journal of pathology.

[31]  W. Streit,et al.  The Microglial Reaction in the Rat Dorsal Hippocampus following Transient Forebrain Ischemia , 1991, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[32]  K. Takakura,et al.  Reduction of delayed neuronal death by inhibition of protein synthesis , 1990, Neuroscience Letters.

[33]  L. Shuer,et al.  Effect of hyperglycemia on neuronal changes in a rabbit model of focal cerebral ischemia. , 1990, Stroke.

[34]  Magnus Thordstein,et al.  Extracellular overflow of glutamate, aspartate, GABA and taurine in the cortex and basal ganglia of fetal lambs during hypoxia-ischemia , 1987, Neuroscience Letters.

[35]  A Gunn,et al.  Time course of intracellular edema and epileptiform activity following prenatal cerebral ischemia in sheep. , 1991, Stroke.