Frances J Northington

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi Neuronal cell death in neonatal hypoxia-ischemia
    Frances J Northington
    Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Ann Neurol 69:743-58. 2011
  2. ncbi Apoptosis in perinatal hypoxic-ischemic brain injury: how important is it and should it be inhibited?
    Frances J Northington
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Dept of Pediatrics, CMSC 6 104, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD 21287, USA
    Brain Res Brain Res Rev 50:244-57. 2005
  3. 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
  4. ncbi Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI
    Frances J Northington
    Neonatal Research Laboratory, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Cereb Blood Flow Metab 31:178-89. 2011
  5. ncbi Antioxidant status alters levels of Fas-associated death domain-like IL-1B-converting enzyme inhibitory protein following neonatal hypoxia-ischemia
    Kurlen S E Payton
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Neonatal Research Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Dev Neurosci 29:403-11. 2007
  6. ncbi Delayed neural network degeneration after neonatal hypoxia-ischemia
    Brian S Stone
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Neonatal Research Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Ann Neurol 64:535-46. 2008
  7. ncbi Inducible nitric oxide synthase is present in motor neuron mitochondria and Schwann cells and contributes to disease mechanisms in ALS mice
    Kevin Chen
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MA 21205 2196, USA
    Brain Struct Funct 214:219-34. 2010
  8. ncbi Effect of hyperoxic exposure during early development on neurotrophin expression in the carotid body and nucleus tractus solitarii
    Raul Chavez-Valdez
    Department of Pediatrics, Division of Neonatology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 3200, USA
    J Appl Physiol 112:1762-72. 2012
  9. ncbi Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury
    Ernest M Graham
    Department of Gyn Ob, Division of Maternal Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neurobiol Dis 17:89-98. 2004
  10. ncbi Large fetal sacrococcygeal teratomas: could early delivery improve outcome?
    Cynthia J Holcroft
    Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Fetal Diagn Ther 24:55-60. 2008

Collaborators

Detail Information

Publications19

  1. ncbi Neuronal cell death in neonatal hypoxia-ischemia
    Frances J Northington
    Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Ann Neurol 69:743-58. 2011
    ..The accurate identification of the various cell death chreodes and their mechanisms unfolding within the immature brain matrix could provide fresh insight for developing meaningful therapies for neonatal and pediatric HIE...
  2. ncbi Apoptosis in perinatal hypoxic-ischemic brain injury: how important is it and should it be inhibited?
    Frances J Northington
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Dept of Pediatrics, CMSC 6 104, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD 21287, USA
    Brain Res Brain Res Rev 50:244-57. 2005
    ..This review summarizes current evidence for apoptotic mechanisms in perinatal brain injury and addresses issues pertinent to the development of antiapoptosis therapies for perinatal HI and stroke...
  3. 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...
  4. ncbi Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI
    Frances J Northington
    Neonatal Research Laboratory, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Cereb Blood Flow Metab 31:178-89. 2011
    ..The effects of necrostatin treatment after HI reflect the importance of necrosis in the delayed phases of neonatal brain injury and represent a new direction for therapy of neonatal HI...
  5. ncbi Antioxidant status alters levels of Fas-associated death domain-like IL-1B-converting enzyme inhibitory protein following neonatal hypoxia-ischemia
    Kurlen S E Payton
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Neonatal Research Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Dev Neurosci 29:403-11. 2007
    ..The mechanism by which antioxidant status alters FLIP levels following neonatal HI may be related to the ability to detoxify H2O2 produced following neonatal HI...
  6. ncbi Delayed neural network degeneration after neonatal hypoxia-ischemia
    Brian S Stone
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Neonatal Research Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Ann Neurol 64:535-46. 2008
    ....
  7. ncbi Inducible nitric oxide synthase is present in motor neuron mitochondria and Schwann cells and contributes to disease mechanisms in ALS mice
    Kevin Chen
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MA 21205 2196, USA
    Brain Struct Funct 214:219-34. 2010
    ..This work identifies two new potential early mechanisms for MN degeneration in mouse ALS involving iNOS at MN mitochondria and Schwann cells and suggests that therapies targeting iNOS might be beneficial in treating human ALS...
  8. ncbi Effect of hyperoxic exposure during early development on neurotrophin expression in the carotid body and nucleus tractus solitarii
    Raul Chavez-Valdez
    Department of Pediatrics, Division of Neonatology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 3200, USA
    J Appl Physiol 112:1762-72. 2012
    ....
  9. ncbi Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury
    Ernest M Graham
    Department of Gyn Ob, Division of Maternal Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neurobiol Dis 17:89-98. 2004
    ..Basal levels of endogenous decoy proteins may modulate the response to Fas death receptor signaling and provide a novel approach to understanding mechanisms of neonatal brain injury...
  10. ncbi Large fetal sacrococcygeal teratomas: could early delivery improve outcome?
    Cynthia J Holcroft
    Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Fetal Diagn Ther 24:55-60. 2008
    ..To determine if gestational age (GA) at delivery or tumor size impacts outcome in neonates with very large sacrococcygeal teratomas (SCTs)...
  11. ncbi Cannabinoid receptor expression in peripheral arterial chemoreceptors during postnatal development
    Gabrielle L McLemore
    Dept of Biology, Morgan State Univ, 1700 East Cold Spring Ln, Baltimore, MD 21251, USA
    J Appl Physiol 97:1486-95. 2004
    ..The novel finding of nuclear localization of CB1Rs in peripheral ganglion cells suggests that these receptors may have an, as yet, undetermined role in nuclear signaling in sensory and autonomic neurons...
  12. ncbi Neonatal brain imaging and the identification of metabolic acidemia and hypoxic-ischemic encephalopathy
    Kristy A Ruis
    Division of Maternal Fetal Medicine, Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 1228, USA
    J Matern Fetal Neonatal Med 22:823-8. 2009
    ..To determine the precision with which intrapartum metabolic acidemia and hypoxic-ischemic encephalopathy (HIE) in term and near-term infants can be identified by neonatal brain imaging...
  13. ncbi Programmed Necrosis: A Prominent Mechanism of Cell Death following Neonatal Brain Injury
    Raul Chavez-Valdez
    Neonatal Research Laboratory, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287 3200, USA
    Neurol Res Int 2012:257563. 2012
    ..There are still more questions than answers, yet the fascinating new perspectives provided by the understanding of programmed necrosis in the developing brain may lay the foundation for new therapies for neonatal HI...
  14. ncbi Glial fibrillary acidic protein as a biomarker for neonatal hypoxic-ischemic encephalopathy treated with whole-body cooling
    Christopher S Ennen
    Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Am J Obstet Gynecol 205:251.e1-7. 2011
    ..Glial fibrillary acidic protein (GFAP) is specific to astrocytes in the central nervous system. We hypothesized that serum GFAP would be increased in neonates with hypoxic-ischemic encephalopathy (HIE) treated with whole-body cooling...
  15. ncbi A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathy
    Ernest M Graham
    Division of Maternal Fetal Medicine, Department of Gynecology Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Am J Obstet Gynecol 199:587-95. 2008
    ..5 of 1000 live births. The proportion of cerebral palsy associated with intrapartum hypoxia-ischemia is 14.5%. The vast majority of cases of cerebral palsy in nonanomalous term infants are not associated with intrapartum hypoxia-ischemia...
  16. ncbi Brief update on animal models of hypoxic-ischemic encephalopathy and neonatal stroke
    Frances J Northington
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    ILAR J 47:32-8. 2006
    ..This review focuses primarily on the newly developed models, recent adaptations to established models, and the studies of functional outcome that have been published since 2000...
  17. ncbi Increased morbidity in severe early intrauterine growth restriction
    Susan W Aucott
    Department of Pediatrics, Division of Neonatology/CSMC 210, Johns Hopkins University, Baltimore, MD 21287-3200, USA
    J Perinatol 24:435-40. 2004
    ..These findings highlight the unique pattern of mortality and morbidity seen in infants with severe early IUGR...
  18. ncbi X chromosome-linked inhibitor of apoptosis protein reduces oxidative stress after cerebral irradiation or hypoxia-ischemia through up-regulation of mitochondrial antioxidants
    Changlian Zhu
    Center for Brain Repair and Rehabilitation, Institute of Neuroscience and Physiology, Goteborg University, Box 432, SE 405 30 Goteborg, Sweden
    Eur J Neurosci 26:3402-10. 2007
    ....
  19. ncbi Reduction of caspase-8 and -9 cleavage is associated with increased c-FLIP and increased binding of Apaf-1 and Hsp70 after neonatal hypoxic/ischemic injury in mice overexpressing Hsp70
    Yasuhiko Matsumori
    Department of Neurological Surgery, University of California, Department of Veterans Affairs Medical Center, San Francisco, CA 94121, USA
    Stroke 37:507-12. 2006
    ....