Articles: traumatic-brain-injuries.
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Autophagy is a process that recycles damaged proteins and organelles. Beclin 1 is involved in the nucleation phase, while p62 is consumed during the elongation phase. We hypothesized that these autophagy biomarkers are increased in cerebrospinal fluid (CSF) after traumatic brain injury (TBI) in children and associated with unfavorable outcome. ⋯ Beclin 1 and p62 are increased in CSF after TBI, suggesting increased autophagy with impairment of, and/or exceeding the capacity for, autophagic flux. The association of increased p62 with unfavorable outcome suggests that autophagy in excess of the capacity to clear degradation products may be deleterious after TBI.
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Journal of neurotrauma · Jun 2017
Amelioration of penetrating ballistic-like brain injury induced cognitive deficits after neuronal differentiation of transplanted human neural stem cells.
Penetrating traumatic brain injury (PTBI) is one of the major cause of death and disability worldwide. Previous studies with penetrating ballistic-like brain injury (PBBI), a PTBI rat model revealed widespread perilesional neurodegeneration, similar to that seen in humans following gunshot wound to the head, which is unmitigated by any available therapies to date. Therefore, we evaluated human neural stem cell (hNSC) engraftment to putatively exploit the potential of cell therapy that has been seen in other central nervous system injury models. ⋯ In a Morris water maze test at 8 weeks post-transplantation, animals with transplants had shorter latency to platform than vehicle-treated animals. However, weak injury-induced cognitive deficits in the control group at the delayed time point confounded benefits of durable engraftment and neuronal differentiation. Therefore, these results justify further studies to progress towards clinical translation of hNSC therapy for PTBI.
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J Musculoskel Neuron · Jun 2017
Impaired fracture healing with high non-union rates remains irreversible after traumatic brain injury in leptin-deficient mice.
Patients with traumatic brain injury (TBI) and long-bone fractures can show increased callus formation. This effect has already been reproduced in wild-type (wt) mice. However, the mechanisms remain poorly understood. ⋯ This study shows that bony bridging is impaired in the present leptin-deficient trauma model. Furthermore, the phenomenon of increased callus formation after TBI could not be reproduced in ob/ob mice, as in wt mice. Our findings suggest that the increased callus formation after TBI may be dependent on leptin signaling.
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Am J Phys Med Rehabil · Jun 2017
Reciprocal Causation Between Functional Independence and Mental Health 1 and 2 Years After Traumatic Brain Injury: A Cross-Lagged Panel Structural Equation Model.
The research attempting to disentangle the directionality of relationships between mental health and functional outcomes after traumatic brain injury (TBI) is growing but has yielded equivocal findings or focused on isolated predictors or isolated outcomes. The purpose of the current study was to use cross-lagged panel and structural equation modeling (SEM) techniques to examine causality between comprehensive indices of mental health (depression, anxiety, and life satisfaction) and functional independence in a national sample of individuals with TBI over the first 2 years after injury. ⋯ Advanced ACCREDITATION: The Association of Academic Physiatrists is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.The Association of Academic Physiatrists designates this activity for a maximum of 1.5 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
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Chronic pain after traumatic brain injury (TBI) is very common, but the mechanisms linking TBI to pain and the pain-related interactions of TBI with peripheral injuries are poorly understood. In these studies we pursued the hypothesis that TBI pain sensitization is associated with histone acetylation in the rat lateral fluid percussion model. Some animals received hindpaw incisions in addition to TBI to mimic polytrauma. ⋯ The inhibition of HAT using curcumin 50 mg/kg s.c reduced mechanical sensitization while the HDAC inhibitor suberoylanilide hydroxamic acid 50 mg/kg i.p. prolonged sensitization in the TBI rats. Immunohistochemical analyses of spinal cord tissue localized changes in the level of acetylation of the H3K9 histone mark to dorsal horn neurons. Taken together, these findings demonstrate that TBI induces sustained nociceptive sensitization, and changes in spinal neuronal histone proteins may play an important role.