L J Martin

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. 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
  2. ncbi request reprint Long-term culture of mouse cortical neurons as a model for neuronal development, aging, and death
    Christian Lesuisse
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurobiol 51:9-23. 2002
  3. ncbi request reprint Adult motor neuron apoptosis is mediated by nitric oxide and Fas death receptor linked by DNA damage and p53 activation
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurosci 25:6449-59. 2005
  4. ncbi request reprint Injury-induced spinal motor neuron apoptosis is preceded by DNA single-strand breaks and is p53- and Bax-dependent
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurobiol 50:181-97. 2002
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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

Collaborators

Detail Information

Publications56

  1. 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...
  2. ncbi request reprint Long-term culture of mouse cortical neurons as a model for neuronal development, aging, and death
    Christian Lesuisse
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurobiol 51:9-23. 2002
    ..These neurons sustain protein nitration during aging and exhibit age-related variations in the biochemistry of neuronal apoptosis...
  3. ncbi request reprint Adult motor neuron apoptosis is mediated by nitric oxide and Fas death receptor linked by DNA damage and p53 activation
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurosci 25:6449-59. 2005
    ..Thus, adult spinal MN apoptosis is mediated by upstream NO and ONOO- genotoxicity and downstream p53 and Fas activation and is shifted to necrosis by mutant SOD1...
  4. ncbi request reprint Injury-induced spinal motor neuron apoptosis is preceded by DNA single-strand breaks and is p53- and Bax-dependent
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurobiol 50:181-97. 2002
    ..We conclude that adult motor neuron death after nerve avulsion is DNA damage-induced, p53- and Bax-dependent apoptosis...
  5. 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
    ....
  6. 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...
  7. 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
    ....
  8. 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
    ....
  9. 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...
  10. 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
    ....
  11. 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...
  12. 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
    ....
  13. 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...
  14. pmc 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...
  15. 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...
  16. 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...
  17. 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
    ....
  18. 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
    ....
  19. 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...
  20. 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...
  21. pmc 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 260:106-19. 2014
    ..The biological significance of ERα predominance and its correlation with BDNF levels is still unclear. ..
  22. 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...
  23. pmc 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...
  24. 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...
  25. 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
    ....
  26. 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...
  27. ncbi request reprint Expression of presenilin 1 and 2 (PS1 and PS2) in human and murine tissues
    M K Lee
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 16:7513-25. 1996
    ..Immunocytochemical studies of mouse brain reveal that PS1 protein accumulates in a variety of neuronal populations with enrichment in somatodendritic and neuropil compartments...
  28. 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
    ....
  29. ncbi request reprint Adult olfactory bulb neural precursor cell grafts provide temporary protection from motor neuron degeneration, improve motor function, and extend survival in amyotrophic lateral sclerosis mice
    Lee J Martin
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 66:1002-18. 2007
    ..OB-NPCs also differentiated into oligodendrocytes and astrocytes that contacted neuronal processes. We conclude that transplantation of adult OB-NPCs is therapeutic for mouse amyotrophic lateral sclerosis...
  30. pmc DNA damage and repair: relevance to mechanisms of neurodegeneration
    Lee J Martin
    Department of Pathology, Division of Neuropathology, and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 67:377-87. 2008
    ..This review summarizes DNA damage and repair mechanisms and their potential relevance to the evolution of degeneration in postmitotic neurons...
  31. ncbi request reprint The adult neural stem and progenitor cell niche is altered in amyotrophic lateral sclerosis mouse brain
    Zhiping Liu
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Comp Neurol 497:468-88. 2006
    ..We conclude that adult mSOD1 ALS mice have abnormalities in forebrain NSCs, but the essential features of NSC/NPCs remained in presymptomatic and symptomatic mice...
  32. pmc Amyotrophic lateral sclerosis 2-deficiency leads to neuronal degeneration in amyotrophic lateral sclerosis through altered AMPA receptor trafficking
    Chen Lai
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892 3707, USA
    J Neurosci 26:11798-806. 2006
    ....
  33. ncbi request reprint Motor neuron degeneration in amyotrophic lateral sclerosis mutant superoxide dismutase-1 transgenic mice: mechanisms of mitochondriopathy and cell death
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Comp Neurol 500:20-46. 2007
    ..The data support roles for oxidative stress, protein nitration and aggregation, and excitotoxicity as participants in the process of MN degeneration caused by mSOD1...
  34. ncbi request reprint Mitochondriopathy in Parkinson disease and amyotrophic lateral sclerosis
    Lee J Martin
    Department of Pathology, Division of Neuropathology and Neuroscience, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, USA
    J Neuropathol Exp Neurol 65:1103-10. 2006
    ..This review presents how malfunctioning mitochondria might contribute to neuronal death in PD and ALS...
  35. pmc Dopamine receptor modulation of hypoxic-ischemic neuronal injury in striatum of newborn piglets
    Zeng Jin Yang
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Cereb Blood Flow Metab 27:1339-51. 2007
    ..Furthermore, mechanisms of D1 receptor toxicity may involve DARPP-32-dependent phosphorylation of NMDA receptor NR1 and Na(+),K(+)-ATPase...
  36. ncbi request reprint Transgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Department of Neuroscience, Johns Hopkins University School ofMedicine, Baltimore, MD 21205 2196, USA
    Rev Neurosci 18:115-36. 2007
    ..These experiments reveal that mitochondrial nitrative stress and perturbations in mitochondrial trafficking may be antecedents of neuronal cell death in animal models of PD and ALS...
  37. ncbi request reprint Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurosci 26:41-50. 2006
    ..Thus, A53T mutant mice develop intraneuronal inclusions, mitochondrial DNA damage and degeneration, and apoptotic-like death of neocortical, brainstem, and motor neurons...
  38. pmc Rapid NMDA receptor phosphorylation and oxidative stress precede striatal neurodegeneration after hypoxic ischemia in newborn piglets and are attenuated with hypothermia
    Dawn Mueller-Burke
    School of Nursing, University of Maryland at Baltimore, Baltimore, MD 21201, USA
    Int J Dev Neurosci 26:67-76. 2008
    ..Postasphyxic, mild whole body hypothermia provides neuroprotection by suppressing N-methyl-d-aspartate receptor phosphorylation and protein oxidation...
  39. ncbi request reprint Motor neuron disease occurring in a mutant dynactin mouse model is characterized by defects in vesicular trafficking
    Fiona M Laird
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 28:1997-2005. 2008
    ..This novel mouse model will be instrumental for not only clarifying disease mechanisms in ALS, but also for testing therapeutic strategies to ameliorate this devastating disease...
  40. ncbi request reprint Transplanted human embryonic germ cell-derived neural stem cells replace neurons and oligodendrocytes in the forebrain of neonatal mice with excitotoxic brain damage
    Dawn Mueller
    Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Neurosci Res 82:592-608. 2005
    ..c) 2005 Wiley-Liss, Inc...
  41. ncbi request reprint 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...
  42. ncbi request reprint Axonal transection in adult rat brain induces transsynaptic apoptosis and persistent atrophy of target neurons
    Stephen D Ginsberg
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurotrauma 19:99-109. 2002
    ..This transneuronal degeneration can be classified as sustained neuronal atrophy or transsynaptic apoptosis...
  43. ncbi request reprint Altered expression and phosphorylation of N-methyl-D-aspartate receptors in piglet striatum after hypoxia-ischemia
    Anne Marie Guerguerian
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Brain Res Mol Brain Res 104:66-80. 2002
    ....
  44. ncbi request reprint Immature and mature cortical neurons engage different apoptotic mechanisms involving caspase-3 and the mitogen-activated protein kinase pathway
    Christian Lesuisse
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Cereb Blood Flow Metab 22:935-50. 2002
    ..The results show that immature and mature cortical neurons engage different signaling mechanisms in MAP kinase and caspase pathways during apoptosis; thus, neuron age influences the mechanisms and progression of apoptosis...
  45. ncbi request reprint Rapid subcellular redistribution of Bax precedes caspase-3 and endonuclease activation during excitotoxic neuronal apoptosis in rat brain
    Josephine Lok
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurotrauma 19:815-28. 2002
    ....
  46. ncbi request reprint DNA base-excision repair enzyme apurinic/apyrimidinic endonuclease/redox factor-1 is increased and competent in the brain and spinal cord of individuals with amyotrophic lateral sclerosis
    Arif Y Shaikh
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Neuromolecular Med 2:47-60. 2002
    ..We conclude that mechanisms for DNA repair are activated in ALS, supporting the possibility that DNA damage is an upstream mechanism for motor neuron degeneration in this disease...
  47. ncbi request reprint DNA damage profiling in motor neurons: a single-cell analysis by comet assay
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurochem Res 27:1093-104. 2002
    ..Viable mature MN can be isolated and used for in vitro models of MN genotoxicity and can be isolated from in vivo models of MN degeneration for profiling DNA damage on a single-cell basis...
  48. ncbi request reprint Early events of target deprivation/axotomy-induced neuronal apoptosis in vivo: oxidative stress, DNA damage, p53 phosphorylation and subcellular redistribution of death proteins
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurochem 85:234-47. 2003
    ....
  49. ncbi request reprint Olfactory bulb core is a rich source of neural progenitor and stem cells in adult rodent and human
    Zhiping Liu
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Comp Neurol 459:368-91. 2003
    ..Cocultured OB-derived neural stem cells with myoblast cells also generated nonneural cell progeny. We conclude that the adult mammalian OB core is a reservoir of neural progenitor cells and pluripotent neural stem cells...
  50. ncbi request reprint Hypothermia for 24 hours after asphyxic cardiac arrest in piglets provides striatal neuroprotection that is sustained 10 days after rewarming
    Dawn M Agnew
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Hospital, Blalock 1404, 600 N Wolfe Street, Baltimore, MD 21287 U S A
    Pediatr Res 54:253-62. 2003
    ....
  51. ncbi request reprint Nitration of the striatal Na,K-ATPase alpha3 isoform occurs in normal brain development but is not increased during hypoxia-ischemia in newborn piglets
    W Christopher Golden
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Neurochem Res 28:1883-9. 2003
    ..Protein nitration may serve as marker of other normal, noninjurious cell processes in the developing brain...
  52. ncbi request reprint Histopathological and behavioral characterization of a novel model of cardiac arrest and cardiopulmonary resuscitation in mice
    Julia Kofler
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, 720 Rutland Avenue, Baltimore, MD 21205, USA
    J Neurosci Methods 136:33-44. 2004
    ..A dissociation between functional and histological outcome was found emphasizing the importance of combining both outcome measures for evaluation of neuroprotective strategies...
  53. ncbi request reprint 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...
  54. ncbi request reprint Pluripotent fates and tissue regenerative potential of adult olfactory bulb neural stem and progenitor cells
    Zhiping Liu
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurotrauma 21:1479-99. 2004
    ....
  55. ncbi request reprint In situ immunoradiographic method for quantification of specific proteins in normal and ischemic brain regions
    Annette Rebel
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    J Neurosci Methods 143:227-35. 2005
    ..The disadvantage of the falsely positive overestimation of protein immunoreactivity after stroke with the immunoperoxidase method has to be weighted with the advantage of the cellular resolution...
  56. pmc Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons
    Miguel Angel Riudavets
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurobiol Aging 28:1484-92. 2007
    ..This nuclear hypertrophy may represent an early neuronal reaction to Abeta or Tau, or a compensatory mechanism which forestalls the progression of AD and allows the brain to resist the development of dementia...