L J Martin

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi request reprint Primary sensory and forebrain motor systems in the newborn brain are preferentially damaged by hypoxia-ischemia
    L J Martin
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    J Comp Neurol 377:262-85. 1997
  2. ncbi request reprint Neuronal death in newborn striatum after hypoxia-ischemia is necrosis and evolves with oxidative stress
    L J Martin
    Department of Pathology, Division of Neuropathy, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Neurobiol Dis 7:169-91. 2000
  3. ncbi request reprint Neurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: A perspective on the contributions of apoptosis and necrosis
    L J Martin
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    Brain Res Bull 46:281-309. 1998
  4. ncbi request reprint Failure to sustain recovery of Na,K-ATPase function is a possible mechanism for striatal neurodegeneration in hypoxic-ischemic newborn piglets
    W C Golden
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Brain Res Mol Brain Res 88:94-102. 2001
  5. ncbi request reprint 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
  6. ncbi request reprint 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
  7. ncbi request reprint 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
  8. ncbi request reprint Motor neurons rapidly accumulate DNA single-strand breaks after in vitro exposure to nitric oxide and peroxynitrite and in vivo axotomy
    Z Liu
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, Maryland 21205-2196, USA
    J Comp Neurol 432:35-60. 2001
  9. doi request reprint 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
  10. ncbi request reprint Protein kinase C expression and activity after global incomplete cerebral ischemia in dogs
    F E Sieber
    Department of Anesthesiology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Stroke 29:1445-52; discussion 1452-3. 1998

Collaborators

Detail Information

Publications24

  1. ncbi request reprint Primary sensory and forebrain motor systems in the newborn brain are preferentially damaged by hypoxia-ischemia
    L J Martin
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    J Comp Neurol 377:262-85. 1997
    ..This distribution of neonatal encephalopathy is dictated possibly by regional function, mitochondrial activity, and connectivity...
  2. ncbi request reprint Neuronal death in newborn striatum after hypoxia-ischemia is necrosis and evolves with oxidative stress
    L J Martin
    Department of Pathology, Division of Neuropathy, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Neurobiol Dis 7:169-91. 2000
    ....
  3. ncbi request reprint Neurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: A perspective on the contributions of apoptosis and necrosis
    L J Martin
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    Brain Res Bull 46:281-309. 1998
    ....
  4. ncbi request reprint Failure to sustain recovery of Na,K-ATPase function is a possible mechanism for striatal neurodegeneration in hypoxic-ischemic newborn piglets
    W C Golden
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Brain Res Mol Brain Res 88:94-102. 2001
    ..We conclude that early inactivation of Na,K-ATPase function participates in the pathogenesis of striatal neuron necrosis, but that loss of enzyme function early after HI is not caused by depletion of composite alpha/beta subunits...
  5. ncbi request reprint 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...
  6. ncbi request reprint 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
    ....
  7. ncbi request reprint 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
    ....
  8. ncbi request reprint Motor neurons rapidly accumulate DNA single-strand breaks after in vitro exposure to nitric oxide and peroxynitrite and in vivo axotomy
    Z Liu
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, Maryland 21205-2196, USA
    J Comp Neurol 432:35-60. 2001
    ..We conclude that motor neurons challenged by oxidative stress and axotomy accumulate DNA-SSB early in their degeneration and that the formation of peroxynitrite is involved in the mechanisms...
  9. doi request reprint 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...
  10. ncbi request reprint Protein kinase C expression and activity after global incomplete cerebral ischemia in dogs
    F E Sieber
    Department of Anesthesiology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Stroke 29:1445-52; discussion 1452-3. 1998
    ..We tested the hypothesis that elevations in the biochemical activity and protein expression of Ca2+-dependent PKC isoforms occur in hippocampus and cerebellum during the period of delayed neurodegeneration after mild brain ischemia...
  11. ncbi request reprint Projection neurons and interneurons in the lateral geniculate nucleus undergo distinct forms of degeneration ranging from retrograde and transsynaptic apoptosis to transient atrophy after cortical ablation in rat
    N A Al-Abdulla
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Neuroscience 115:7-14. 2002
    ..Nevertheless, a small subset of lateral geniculate interneurons undergoes transsynaptic apoptosis in response to projection neuron apoptosis. The pathological responses of thalamic neurons to cortical trauma vary depending on cell type...
  12. ncbi request reprint Neuronal cell death in nervous system development, disease, and injury (Review)
    L J Martin
    Johns Hopkins University School of Medicine, Department of Pathology, Baltimore, MD 21205 2196, USA
    Int J Mol Med 7:455-78. 2001
    ....
  13. pmc Mitochondrial toxin 3-nitropropionic acid induces cardiac and neurotoxicity differentially in mice
    K L Gabrielson
    Division of Comparative Medicine, School of Medicine, School of Medicine, The Johns Hopkins University, Baltimore, Maryland, USA
    Am J Pathol 159:1507-20. 2001
    ....
  14. ncbi request reprint Low-dose ouabain protects against excitotoxic apoptosis and up-regulates nuclear Bcl-2 in vivo
    W C Golden
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Nelson Harvey 2 133, Baltimore, MD 21287, USA
    Neuroscience 137:133-44. 2006
    ..Targeted, therapeutic inhibition of apoptosis through cardiac glycosides may represent an effective strategy against excitotoxicity-mediated neuronal injury...
  15. ncbi request reprint 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...
  16. ncbi request reprint 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
    ....
  17. ncbi request reprint Cognitive decline strongly correlates with cortical atrophy in Alzheimer's dementia
    P R Mouton
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurobiol Aging 19:371-7. 1998
    ..These findings confirm fundamental differences in the temporal patterns of cortical volume loss in aging and AD, and support cortical degeneration as the primary basis for cognitive decline in AD...
  18. ncbi request reprint Ontogeny of non-NMDA glutamate receptors in rat barrel field cortex: I. Metabotropic receptors
    M E Blue
    The Kennedy Krieger Research Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Comp Neurol 386:16-28. 1997
    ..We conclude from the developmental localization of mGluRs that the spatiotemporal regulated expression of these receptors may influence barrel maturation and plasticity...
  19. ncbi request reprint Sexual dimorphism in BDNF signaling after neonatal hypoxia-ischemia and treatment with necrostatin-1
    R Chavez-Valdez
    Department of Pediatrics, Neonatal Research Laboratory, Johns Hopkins University School of Medicine, 600 North Wolfe Street, CMSC 6 104, Baltimore, MD 21287, USA Electronic address
    Neuroscience . 2013
    ..The biological significance of ERα predominance and its correlation with BDNF levels is still unclear...
  20. ncbi request reprint Isolation of mature spinal motor neurons and single-cell analysis using the comet assay of early low-level DNA damage induced in vitro and in vivo
    Z Liu
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Histochem Cytochem 49:957-72. 2001
    ..Using these methods, we conclude that motor neurons undergoing oxidative stress from reactive oxygen species and axotomy accumulate DNA damage early in their degeneration...
  21. pmc Effect of glutamine synthetase inhibition on astrocyte swelling and altered astroglial protein expression during hyperammonemia in rats
    H Tanigami
    Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, 600 North Wolfe Street Blalock 1404, Baltimore, MD 21287 4961, USA
    Neuroscience 131:437-49. 2005
    ....
  22. ncbi request reprint Injury-induced apoptosis of neurons in adult brain is mediated by p53-dependent and p53-independent pathways and requires Bax
    L J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Comp Neurol 433:299-311. 2001
    ..Neuronal apoptosis in the dorsal LGN is blocked completely in bax(-/-) mice. We conclude that neuronal apoptosis in the adult thalamus after cortical injury requires Bax and is modulated by p53...
  23. ncbi request reprint Selective regional loss of exocytotic presynaptic vesicle proteins in Alzheimer's disease brains
    C I Sze
    Department of Pathology, University of Colorado Health Sciences Center, B 216, 4200 East Ninth Ave, Denver, CO 80262, USA
    J Neurol Sci 175:81-90. 2000
    ..These results suggest that there are selective and early defects in presynaptic vesicle proteins, but not synaptic plasma membrane proteins in AD and that defects correlate with cognitive dysfunction in this disease...
  24. ncbi request reprint Neuronal disorders: studies of animal models and human diseases
    D L Price
    Neuropathology Laboratory, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2181
    Toxicol Pathol 18:128-37. 1990
    ....