F J Northington
Affiliation: Johns Hopkins University
- Nitric oxide synthase 1 and nitric oxide synthase 3 protein expression is regionally and temporally regulated in fetal brainF J Northington
Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
Brain Res Dev Brain Res 95:1-14. 1996....
- Delayed neurodegeneration in neonatal rat thalamus after hypoxia-ischemia is apoptosisF J Northington
Eudowood Neonatal Pulmonary Division, Department of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
J Neurosci 21:1931-8. 2001..We conclude that the delayed neurodegeneration in neonatal rat ventral basal thalamus after hypoxic-ischemic injury is apoptosis mediated by death receptor activation...
- Neurodegeneration in the thalamus following neonatal hypoxia-ischemia is programmed cell deathF J Northington
Eudowood Neonatal Pulmonary Division, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Dev Neurosci 23:186-91. 2001....
- Early Neurodegeneration after Hypoxia-Ischemia in Neonatal Rat Is Necrosis while Delayed Neuronal Death Is ApoptosisF J Northington
Departments of Pediatrics, Eudowood Neonatal Pulmonary Division, Baltimore, Maryland 21287, USA
Neurobiol Dis 8:207-19. 2001....
- Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as "continuum" phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrainF J Northington
Department of Pediatrics, CMSC 6 104, The Johns Hopkins University School of Medicine, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21287, USA
Neuroscience 149:822-33. 2007..The presence of a "continuum" phenotype of cell death that varies on a cell-by-cell basis suggests that the phenotype of cell death is dependent on the energy available to drive the apoptotic pathways to completion...
- Necrostatin-1 attenuates mitochondrial dysfunction in neurons and astrocytes following neonatal hypoxia-ischemiaR Chavez-Valdez
Department of Pediatrics, Division of Neonatology, Johns Hopkins Medical Institutions, Johns Hopkins Hospital, 600 N Wolfe Street, CMSC 6 104, Baltimore, MD 21287, USA
Neuroscience 219:192-203. 2012..We conclude that Nec-1 immediately after HI, is strongly mitoprotective and prevents secondary energy failure by blocking early NO• accumulation, glutathione oxidation and attenuating mitochondrial dysfunction...
- Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitiveR N Ichord
Departments of Neurology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
Am J Physiol 276:H2053-62. 1999..EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycemic coma in the immature brain, CMRO2 and glutamate are increased in a temperature-dependent manner...