F J Northington

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi Nitric oxide synthase 1 and nitric oxide synthase 3 protein expression is regionally and temporally regulated in fetal brain
    F J Northington
    Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
    Brain Res Dev Brain Res 95:1-14. 1996
  2. ncbi Delayed neurodegeneration in neonatal rat thalamus after hypoxia-ischemia is apoptosis
    F 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
  3. ncbi Neurodegeneration in the thalamus following neonatal hypoxia-ischemia is programmed cell death
    F J Northington
    Eudowood Neonatal Pulmonary Division, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Dev Neurosci 23:186-91. 2001
  4. ncbi Early Neurodegeneration after Hypoxia-Ischemia in Neonatal Rat Is Necrosis while Delayed Neuronal Death Is Apoptosis
    F J Northington
    Departments of Pediatrics, Eudowood Neonatal Pulmonary Division, Baltimore, Maryland 21287, USA
    Neurobiol Dis 8:207-19. 2001
  5. ncbi 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 forebrain
    F 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
  6. ncbi Necrostatin-1 attenuates mitochondrial dysfunction in neurons and astrocytes following neonatal hypoxia-ischemia
    R 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
  7. ncbi Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive
    R N Ichord
    Departments of Neurology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
    Am J Physiol 276:H2053-62. 1999

Detail Information

Publications7

  1. ncbi Nitric oxide synthase 1 and nitric oxide synthase 3 protein expression is regionally and temporally regulated in fetal brain
    F J Northington
    Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
    Brain Res Dev Brain Res 95:1-14. 1996
    ....
  2. ncbi Delayed neurodegeneration in neonatal rat thalamus after hypoxia-ischemia is apoptosis
    F 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...
  3. ncbi Neurodegeneration in the thalamus following neonatal hypoxia-ischemia is programmed cell death
    F J Northington
    Eudowood Neonatal Pulmonary Division, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Dev Neurosci 23:186-91. 2001
    ....
  4. ncbi Early Neurodegeneration after Hypoxia-Ischemia in Neonatal Rat Is Necrosis while Delayed Neuronal Death Is Apoptosis
    F J Northington
    Departments of Pediatrics, Eudowood Neonatal Pulmonary Division, Baltimore, Maryland 21287, USA
    Neurobiol Dis 8:207-19. 2001
    ....
  5. ncbi 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 forebrain
    F 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...
  6. ncbi Necrostatin-1 attenuates mitochondrial dysfunction in neurons and astrocytes following neonatal hypoxia-ischemia
    R 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...
  7. ncbi Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive
    R 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...