Journal of neurotrauma
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Journal of neurotrauma · Oct 2006
Traumatic brain injury produces delay-dependent memory impairment in rats.
Memory impairment following traumatic brain injury (TBI) is common in both humans and animals. A noteworthy feature of memory dysfunction in human TBI is impaired memory performance that is dependent on the delay between initial learning and recall of information. However, previous studies of TBI-induced memory impairment in animals have failed to control for the initial amount of learning between sham and injured animals. ⋯ However, as the delay increased to 30 and 120 sec, the performance of the injured animals deteriorated (p < 0.05). These results indicate that LFP injury produces delay-dependent memory impairments in rats. This is therefore a valid model of an important feature of memory impairment in human TBI, and should be a useful addition to the available methods for assessing memory impairment and the effect of therapeutic interventions after TBI.
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Journal of neurotrauma · Sep 2006
Neuronal response to high rate shear deformation depends on heterogeneity of the local strain field.
Many cellular models of traumatic brain injury (TBI) deform cells in a planar (2-D) configuration, a contrast from the three-dimensional (3-D) architecture of the brain, resulting in strain fields that may fail to represent the complex deformation patterns seen in vivo. Cells cultured in 3-D may more accurately represent in vivo cellular behavior than planar models due to differences in cytostructure, cell-cell/cell-matrix interactions and access to trophic factors; however, the effects of culture configuration on the response to high rate deformation have not been evaluated. We examined cell viability following a defined mechanical insult to primary cortical neurons distributed throughout a bioactive matrix (3-D) or in a monolayer sandwiched between layers of a bioactive matrix (2-D). ⋯ Computer simulations of bulk loading predicted local cellular strains, revealing that neurons in 3-D were subjected to a heterogeneous strain field simultaneously consisting of tensile, compressive and shear strains; conversely, neurons in 2-D experienced a less complex deformation regime varying mainly based on shear strains. These results show differential susceptibility to mechanical loading between neurons cultured in 2-D and 3-D that may be due to differences in cellular strain manifestation. Models of TBI that accurately represent the related cellular biomechanics and pathophysiology are important for the elucidation of cellular tolerances and the development of mechanistically driven intervention strategies.
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Journal of neurotrauma · Sep 2006
Activin a release into cerebrospinal fluid in a subset of patients with severe traumatic brain injury.
Activin A is a member of the transforming growth factor-beta superfamily and has been demonstrated to be elevated during inflammation and to have neuroprotective properties following neural insults. In this study, we examined whether traumatic brain injury (TBI) induced a response in activin A or in the concentrations of its binding protein, follistatin. Thirty-nine patients with severe TBI had daily, matched cerebrospinal fluid (CSF) and serum samples collected post-TBI and these were assayed for activin A and follistatin using specific immunoassays. ⋯ Further, activin A levels were also associated with indices of metabolism, such as lactate and pyruvate, excitotoxicity (glutamate) and membrane lipid breakdown products such as glycerol. In one of the two patients who developed a CSF infection, activin A concentrations in CSF became markedly elevated. Thus, some TBI patients have an early release of activin A into the CSF that may result from activation of inflammatory and/or neuroprotective pathways.
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Journal of neurotrauma · Sep 2006
Comparative StudyTransplantation of bone marrow stem cells as well as mobilization by granulocyte-colony stimulating factor promotes recovery after spinal cord injury in rats.
Emerging clinical studies of treating brain and spinal cord injury (SCI) with autologous adult stem cells led us to compare the effect of an intravenous injection of mesenchymal stem cells (MSCs), an injection of a freshly prepared mononuclear fraction of bone marrow cells (BMCs) or bone marrow cell mobilization induced by granulocyte colony stimulating factor (G-CSF) in rats with a balloon- induced spinal cord compression lesion. MSCs were isolated from rat bone marrow by their adherence to plastic, labeled with iron-oxide nanoparticles and expanded in vitro. Seven days after injury, rats received an intravenous injection of MSCs or BMCs or a subcutaneous injection of GCSF (from day 7 to 11 post-injury). ⋯ The lesions populated by grafted MSCs appeared as dark hypointense areas. Histology confirmed a large number of iron-containing and PKH 26-positive cells in the lesion site. We conclude that treatment with three different bone marrow cell populations had a positive effect on behavioral outcome and histopathological assessment after SCI, which was most pronounced after MSC injection.
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Journal of neurotrauma · Aug 2006
Review Meta AnalysisSerum biochemical markers for post-concussion syndrome in patients with mild traumatic brain injury.
Mild traumatic brain injury (MTBI) is a major public health problem in the United States. A significant subset of MTBI patients develop persistent and distressing neurological, cognitive, and behavioral symptoms, known as the post-concussion syndrome (PCS). To date, multiple studies have assessed the relationship between brain-related proteins found in the serum at the time of injury, and the development of PCS. ⋯ Of these markers, S100 appeared to be the best researched. We conclude that no biomarker has consistently demonstrated the ability to predict PCS after MTBI. A combination of clinical factors in conjunction with biochemical markers may be necessary to develop a comprehensive decision rule that more accurately predicts PCS after MTBI.