R Raghupathi

Summary

Affiliation: University of Pennsylvania
Country: USA

Publications

  1. ncbi request reprint Mild traumatic brain injury induces apoptotic cell death in the cortex that is preceded by decreases in cellular Bcl-2 immunoreactivity
    R Raghupathi
    Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    Neuroscience 110:605-16. 2002
  2. ncbi request reprint Apoptosis after traumatic brain injury
    R Raghupathi
    Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    J Neurotrauma 17:927-38. 2000
  3. pmc Brain trauma induces massive hippocampal neuron death linked to a surge in beta-amyloid levels in mice overexpressing mutant amyloid precursor protein
    D H Smith
    Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104 6316, USA
    Am J Pathol 153:1005-10. 1998
  4. ncbi request reprint The maxi-K channel opener BMS-204352 attenuates regional cerebral edema and neurologic motor impairment after experimental brain injury
    J A Cheney
    Department of Neurosurgery, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Cereb Blood Flow Metab 21:396-403. 2001
  5. ncbi request reprint Effects of chronic, post-injury Cyclosporin A administration on motor and sensorimotor function following severe, experimental traumatic brain injury
    P Riess
    Department of Neurosurgery, School of Medicine, University of Pennsylvania, 3320 Smith Walk, Philadelphia PA 19104, USA
    Restor Neurol Neurosci 18:1-8. 2001
  6. ncbi request reprint A review and rationale for the use of genetically engineered animals in the study of traumatic brain injury
    L Longhi
    Department of Neurosurgery, University of Pennsylvania and Veterans Administration Medical Center, Philadelphia, Pennsylvania 19104, USA
    J Cereb Blood Flow Metab 21:1241-58. 2001
  7. ncbi request reprint Mild head injury increasing the brain's vulnerability to a second concussive impact
    H L Laurer
    The Head Injury Center, Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104-6316, USA
    J Neurosurg 95:859-70. 2001
  8. ncbi request reprint DNase I disinhibition is predominantly associated with actin hyperpolymerization after traumatic brain injury
    F M Bareyre
    Department of Neurosurgery, University of Pennsylvania, Philadelphia, USA
    J Neurochem 77:173-81. 2001
  9. ncbi request reprint Age-related differences in acute physiologic response to focal traumatic brain injury in piglets
    S R Durham
    Department of Neurosurgery, University of Pennsylvania School of Medicine, The Children s Hospital of Philadelphia, Philadelphia, PA, USA
    Pediatr Neurosurg 33:76-82. 2000
  10. ncbi request reprint Pharmacologic inhibition of poly(ADP-ribose) polymerase is neuroprotective following traumatic brain injury in rats
    M C LaPlaca
    Department of Neurosurgery, University of Pennsylvania, Philadelphia, USA
    J Neurotrauma 18:369-76. 2001

Collaborators

Detail Information

Publications21

  1. ncbi request reprint Mild traumatic brain injury induces apoptotic cell death in the cortex that is preceded by decreases in cellular Bcl-2 immunoreactivity
    R Raghupathi
    Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    Neuroscience 110:605-16. 2002
    ....
  2. ncbi request reprint Apoptosis after traumatic brain injury
    R Raghupathi
    Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    J Neurotrauma 17:927-38. 2000
    ..Finally, in light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain...
  3. pmc Brain trauma induces massive hippocampal neuron death linked to a surge in beta-amyloid levels in mice overexpressing mutant amyloid precursor protein
    D H Smith
    Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104 6316, USA
    Am J Pathol 153:1005-10. 1998
    ..01). These data suggest a mechanistic link between brain trauma and Abeta levels and the death of neurons...
  4. ncbi request reprint The maxi-K channel opener BMS-204352 attenuates regional cerebral edema and neurologic motor impairment after experimental brain injury
    J A Cheney
    Department of Neurosurgery, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Cereb Blood Flow Metab 21:396-403. 2001
    ..05). No effects on cognitive function or cortical tissue loss were observed with either dose. These results suggest that the novel maxi-K channel opener BMS-204352 may be selectively beneficial in the treatment of experimental TBI...
  5. ncbi request reprint Effects of chronic, post-injury Cyclosporin A administration on motor and sensorimotor function following severe, experimental traumatic brain injury
    P Riess
    Department of Neurosurgery, School of Medicine, University of Pennsylvania, 3320 Smith Walk, Philadelphia PA 19104, USA
    Restor Neurol Neurosci 18:1-8. 2001
    ..CONCLUSION: These data suggest that daily post-injury treatment with CsA improves certain aspects of motor and sensorimotor function following experimental TBI...
  6. ncbi request reprint A review and rationale for the use of genetically engineered animals in the study of traumatic brain injury
    L Longhi
    Department of Neurosurgery, University of Pennsylvania and Veterans Administration Medical Center, Philadelphia, Pennsylvania 19104, USA
    J Cereb Blood Flow Metab 21:1241-58. 2001
    ....
  7. ncbi request reprint Mild head injury increasing the brain's vulnerability to a second concussive impact
    H L Laurer
    The Head Injury Center, Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104-6316, USA
    J Neurosurg 95:859-70. 2001
    ..CONCLUSIONS: On the basis of their results, the authors suggest that the brain has an increased vulnerability to a second traumatic insult for at least 24 hours following an initial episode of mild brain trauma...
  8. ncbi request reprint DNase I disinhibition is predominantly associated with actin hyperpolymerization after traumatic brain injury
    F M Bareyre
    Department of Neurosurgery, University of Pennsylvania, Philadelphia, USA
    J Neurochem 77:173-81. 2001
    ..Collectively our data suggest that DNase I disinhibition following brain trauma is associated predominantly with actin hyperpolymerization but also with actin depolymerization and concomitant caspase-mediated actin proteolysis...
  9. ncbi request reprint Age-related differences in acute physiologic response to focal traumatic brain injury in piglets
    S R Durham
    Department of Neurosurgery, University of Pennsylvania School of Medicine, The Children s Hospital of Philadelphia, Philadelphia, PA, USA
    Pediatr Neurosurg 33:76-82. 2000
    ..The goal of the present study was to determine whether age-related differences in the acute physiologic response to scaled cortical impact injury contribute to differences in vulnerability to traumatic brain injury (TBI)...
  10. ncbi request reprint Pharmacologic inhibition of poly(ADP-ribose) polymerase is neuroprotective following traumatic brain injury in rats
    M C LaPlaca
    Department of Neurosurgery, University of Pennsylvania, Philadelphia, USA
    J Neurotrauma 18:369-76. 2001
    ..The observed neuroprotective effects on lesion size, however, offer a promising option for further evaluation of PARP inhibition as a means to reduce cellular damage associated with TBI...
  11. ncbi request reprint Remacemide hydrochloride reduces cortical lesion volume following brain trauma in the rat
    D H Smith
    Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104 6316, USA
    Neurosci Lett 231:135-8. 1997
    ..v. 15 min postinjury plus a subcutaneous infusion over 24 h of 20 mg/kg remacemide hydrochloride improved posttraumatic memory function determined by a Morris water maze paradigm...
  12. ncbi request reprint Traumatic brain injury in young, amyloid-beta peptide overexpressing transgenic mice induces marked ipsilateral hippocampal atrophy and diminished Abeta deposition during aging
    Y Nakagawa
    The Center for Neurodegenerative Disease Research, Division of Anatomic Pathology, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4283, USA
    J Comp Neurol 411:390-8. 1999
    ....
  13. pmc Prolonged cyclooxygenase-2 induction in neurons and glia following traumatic brain injury in the rat
    K I Strauss
    Department of Neurosurgery, Temple University School of Medicine, Philadelphia, Pennsylvania, USA
    J Neurotrauma 17:695-711. 2000
    ..These may cause secondary injuries to the brain that promote neuropathology and worsen behavioral outcome...
  14. ncbi request reprint Bilateral growth-related protein expression suggests a transient increase in regenerative potential following brain trauma
    D L Emery
    Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Comp Neurol 424:521-31. 2000
    ..Taken together, these results suggest the existence of a temporary posttraumatic state in which the CNS may have increased regenerative potential. Enhancement of such a response may be one therapeutic strategy in treating CNS injury...
  15. ncbi request reprint The assessment of genomic alterations using DNA arrays following traumatic brain injury: a review
    P Marciano
    Department of Neuroscience, University of Pennsylvania, Philadelphia, PA 19104 6316, USA
    Restor Neurol Neurosci 18:105-13. 2001
    ..This review focuses on the technical aspects of microarray manufacture (photolithography, microspotting, and ink jet technology) and their utility in elucidating the molecular sequelae of brain injury...
  16. pmc Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury
    U Scherbel
    Department of Neurosurgery, School of Medicine, University of Pennsylvania, Philadelphia PA 19104, USA
    Proc Natl Acad Sci U S A 96:8721-6. 1999
    ..02). Our results suggest that although the presence of TNF in the acute posttraumatic period may be deleterious, this cytokine may play a role in facilitating long-term behavioral recovery and histological repair after brain injury...
  17. ncbi request reprint Maturation-dependent response of the piglet brain to scaled cortical impact
    A C Duhaime
    Department of Neurosurgery, The Children s Hospital of Philadelphia, University of Pennsylvania School of Medicine, 19104, USA
    J Neurosurg 93:455-62. 2000
    ....
  18. ncbi request reprint Age does not influence DNA fragmentation in the hippocampus after fatal traumatic brain injury in young and aged humans compared with controls
    J Fowler
    University Department of Neuropathology, South Glasgow University Hospitals NHS Trust, Southern General Hospital, UK
    Clin Neuropathol 21:156-62. 2002
    ....
  19. ncbi request reprint In situ DNA fragmentation occurs in white matter up to 12 months after head injury in man
    S Williams
    University Department of Neuropathology, Institute of Neurological Sciences, South Glasgow University Hospitals, NHS Trust, Southern General Hospital, 1345 Govan Road, Glasgow G51 4TF, UK
    Acta Neuropathol 102:581-90. 2001
    ..It was concluded that, as reflected by TUNEL histochemistry, long-term DNA fragmentation is present in white matter after traumatic brain injury in man...
  20. ncbi request reprint No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans
    V E Johnson
    Academic Unit of Neuropathology, University of Glasgow, Glasgow, Scotland, UK
    Clin Neuropathol 25:255-64. 2006
    ..The cellular and molecular responses after head injury are partly influenced by genetic polymorphisms of apolipoprotein E and the pro-inflammatory cytokine IL-I...
  21. ncbi request reprint TUNEL-positive staining in white and grey matter after fatal head injury in man
    K Shaw
    University Department of Neuropathology, South Glasgow University Hospitals NHS Trust, Southern General Hospital, UK
    Clin Neuropathol 20:106-12. 2001
    ..In the grey matter, most TUNEL+ cells had the morphology of necrosis. However, the histological appearances of some of the neurons (2-3%), and of oligodendroglia and macrophages in white matter (about 5%) were those of apoptosis...