Journal of neurotrauma
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Journal of neurotrauma · Nov 2012
Arachidonic acid: a bridge between traumatic brain injury and fracture healing.
Traumatic brain injury (TBI) is associated with enhanced osteogenesis. The aim of this study was to investigate the effect of serum from TBI rats on fracture healing. Results from this study showed that the serum from TBI rats enhanced the expression of bone gamma carboxyglutamate protein (BGLAP), and promoted in vitro proliferation of MC3T3-E1 cells, a mouse osteoblastic cell line. ⋯ Finally, we examined the effects of AA on BGLAP expression and cell proliferation in MC3T3-E1 cells. We found that BGLAP expression and proliferation of osteoblasts were positively regulated in the presence of AA. These findings suggest that the increased AA in serum after TBI may play a key role in enhancing the speed of fracture healing.
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Journal of neurotrauma · Nov 2012
Decreased spinothalamic and dorsal column medial lemniscus-mediated function is associated with neuropathic pain after spinal cord injury.
Neuropathic pain (NP) after spinal cord injury (SCI) can significantly and negatively affect quality of life and is often refractory to currently available treatments. In order to find more effective therapeutic avenues, it would be helpful to identify the primary underlying pathophysiological mechanisms in each individual. The aim of the present study was to assess the relationship between the presence and severity of NP after SCI and measures of somatosensory function mediated via the dorsal column medial lemniscal (DCML) pathway and the spinothalamic tract (STT). ⋯ Our results suggest that both impaired STT and DCML-mediated function are necessary for the development of NP after SCI. However, within the SCI-NP group, greater NP severity was associated with greater sensitivity to thermal stimuli below the LOI. This finding concurs with other studies suggesting that STT damage with some sparing is associated with NP.
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Journal of neurotrauma · Nov 2012
Deficits in social behavior emerge during development after pediatric traumatic brain injury in mice.
The pediatric brain may be particularly vulnerable to social deficits after traumatic brain injury (TBI) due to the protracted nature of psychosocial development through adolescence. However, the majority of pre-clinical studies fail to assess social outcomes in experimental pediatric TBI. The current study evaluated social behavior in mice subjected to TBI at post-natal day (p)21. ⋯ Together these findings reveal reduced social interaction and a tendency towards increased aggression, which evolves across development to adulthood. This emergence of aberrant social behavior, which parallels the development of other cognitive deficits in this model and behaviors seen in brain-injured children, is consistent with the hypothesis that the full extent of deficits is not realized until the associated skills reach maturity. Thus, efficacy of therapeutics for pediatric TBI should take into account the time-dependent emergence of abnormal behavioral patterns.
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Journal of neurotrauma · Nov 2012
Multivariate outcome prediction in traumatic brain injury with focus on laboratory values.
Traumatic brain injury (TBI) is a major cause of morbidity and mortality. Identifying factors relevant to outcome can provide a better understanding of TBI pathophysiology, in addition to aiding prognostication. Many common laboratory variables have been related to outcome but may not be independent predictors in a multivariate setting. ⋯ A worse outcome related to increasing osmolarity may warrant further study. Importantly, hemoglobin was not found significant when adjusted for post-resuscitation GCS as opposed to an admission GCS, and timing of GCS can thus have a major impact on conclusions. In total, laboratory variables added an additional 1.3-4.4% to pseudo R².
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Journal of neurotrauma · Nov 2012
Cerebellar gene expression following human traumatic brain injury.
Gene expression of specific brain biomarkers offers the possibility of shedding light on the difficult molecular pathways of traumatic brain injury (TBI) and may be useful to estimate the age of trauma. Gene expression rates of cerebellar injuries are not yet sufficiently established. In 12 cases (mean age 42 years) of TBI including a pathological change in cerebellum (with known survival times ranging from immediate death to 96 h), brain tissue samples from different brain regions were analyzed with real-time polymerase chain reaction (PCR) for expression of caspase-3, tyrosine kinase receptor B (TrkB), S100B, and glial fibrillary acidic protein (GFAP) mRNA. ⋯ For short survival times, the expression changes of caspase-3 (p<0.05) and the expression changes of TrkB (p<0.1) in the cerebellum show a significant increase compared to the controls. The cerebellar gene expression changes seem to occur much faster and stronger compared to the other investigated regions, in particular the cerebral trauma site. These findings could make the cerebellum an important target area to study the expression changes after TBI.