Articles: traumatic-brain-injuries.
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Adenosine kinase facilitated astrogliosis-induced cortical neuronal death in traumatic brain injury.
Adenosine kinase (ADK) plays a pivotal role in regulating brain function by regulating adenosine level, and ADK inhibition protects against neuronal damage in cerebral ischemia and epilepsy; however, the effects of ADK in traumatic brain injury (TBI) have not been investigated. For exploring its effects, we generated a blade-induced rat focal brain injury model. Western blot analysis, immunohistochemistry and immunofluorescent staining suggested that ADK was up-regulated after TBI, and it was temporally and spatially associated with astrogliosis. ⋯ Additionally, ADK knock-down didn't ameliorate LPS-induced astrocyte proliferation, but it protected against neuronal death by reducing iNOS expression, tumor necrosis factor α and interleukin 1β secretion of reactive astrocytes. Taken together, ADK was associated with astrogliosis after TBI, its inhibition in reactive astrocytes ameliorated astrogliosis-induced neuronal death. Our findings extended the current knowledge on the role of ADK in astrogliosis, and also provided new evidence for the TBI treatment.
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The objective of this study is to present a case series of nonmissile penetrating (NMP) injuries and to establish a workflow for an uncommon mechanism of traumatic head injury through the analysis of each case, classification of the type of lesion, management, and outcome score at follow-up. ⋯ TBIs caused by NMP objects are unusual and caused by aggression, self-inflicted harm (in the case of psychiatric patients), and accident. The foreign body may enter into the skull through a natural hole (orbit, nose, mouth, or ear) or crosses the skull, causing a fracture and creating an artificial hole. Preoperative neuroradiologic assessment is paramount for the correct neurosurgical approach. The main prognostic factor for these patients is the GCS score at admission.
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Journal of neurotrauma · Jun 2016
Fractalkine receptor deficiency is associated with early protection, but late worsening of outcome following brain trauma in mice.
An impaired ability to regulate microglia activation by fractalkine (CX3CL1) leads to microglia chronic sub-activation. How this condition affects outcome after acute brain injury is still debated, with studies showing contrasting results depending on the timing and the brain pathology. Here, we investigated the early and delayed consequences of fractalkine receptor (CX3CR1) deletion on neurological outcome and on the phenotypical features of the myeloid cells present in the lesions of mice with traumatic brain injury (TBI). ⋯ Gene expression on CD11b(+) sorted cells revealed an increase of interleukin 10 and insulin-like growth factor 1 (IGF1) at 1 day and a decrease of IGF1 4 days and 5 weeks post-TBI in CX3CR1(-/-), compared with WT mice. These data show an early protection followed by a chronic exacerbation of TBI outcome in the absence of CX3CR1. Thus, longitudinal effects of myeloid cell manipulation at different stages of pathology should be investigated to understand how and when their modulation may offer therapeutic chances.