Journal of neurotrauma
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Journal of neurotrauma · Jul 2017
Changes in apparent fibre density and track-weighted imaging metrics in white matter following experimental traumatic brain injury.
Traumatic brain injury (TBI) has been assessed with diffusion tensor imaging (DTI), a commonly used magnetic resonance imaging (MRI) marker for white matter integrity. However, given that the DTI model only fits a single fiber orientation, results can become confounded in regions of "crossing" white matter fibers. In contrast, constrained spherical deconvolution estimates a fiber orientation distribution directly from high angular resolution diffusion-weighted images. ⋯ However, the latter DTI metrics identified fewer voxels affected by TBI. Additionally, analysis of AFD with connectivity-based fixel enhancement was the only method that identified damage within the corticospinal tract of rats given an FPI. These results support the use of constrained spherical deconvolution, in conjunction with DTI metrics, to better assess disease progression and treatment post-TBI.
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Journal of neurotrauma · Jul 2017
Clinical Evaluation of a Microwave-Based Device for Detection of Traumatic Intracranial Hemorrhage.
Traumatic brain injury (TBI) is the leading cause of death and disability among young persons. A key to improve outcome for patients with TBI is to reduce the time from injury to definitive care by achieving high triage accuracy. Microwave technology (MWT) allows for a portable device to be used in the pre-hospital setting for detection of intracranial hematomas at the scene of injury, thereby enhancing early triage and allowing for more adequate early care. ⋯ At 100% sensitivity, the specificity was 75%-i.e., all hematomas were detected at the cost of 25% false positives (patients who would be overtriaged). Considering the need for methods to identify patients with intracranial hematomas in the pre-hospital setting, MWT shows promise as a tool to improve triage accuracy. Further studies are under way to evaluate MWT in patients with other intracranial hemorrhages.
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Journal of neurotrauma · Jul 2017
ERK/Nrf2/HO-1 Pathway-Mediated Mitophagy Alleviates Traumatic Brain Injury-Induced Intestinal Mucosa Damage and Epithelial Barrier Dysfunction.
Gastrointestinal dysfunction is one of several physiologic complications in patients with traumatic brain injury (TBI). TBI can result in increased intestinal permeability resulting from apoptosis of intestinal epithelial cells, which contain a large number of mitochondria for persisting barrier function. Autophagy of damaged mitochondria (mitophagy) controls the quality of the mitochondria and regulates cellular homeostasis. ⋯ Additionally, CCI-induced mitophagy was shown to be mediated by the oxidative stress-related extracellular signal-regulated kinase (ERK)/nuclear factor-erythroid2-like2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway, which may serve to reduce the apoptosis induced by oxidative stress. These results suggest that CCI-induced mitophagy serves to diminish apoptosis-mediated intestinal epithelial cell damage and to improve intestinal permeability, via ERK/Nrf2/HO-1 signaling. These findings may be useful in the design of rational approaches for the prevention and treatment of symptoms associated with TBI.
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Journal of neurotrauma · Jul 2017
Alteration in long non-coding RNA expression after traumatic brain injury in rats.
Traumatic brain injury (TBI) causes a primary insult and initiates a secondary injury cascade. The mechanisms underlying the secondary injury are multifactorial and may include the aberrant expression of long non-coding RNA (lncRNA) post-TBI. Here, lncRNA microarray analysis was performed to profile the altered lncRNAs in the rat hippocampus after TBI. ⋯ Sub-co-expression networks were formed for the top three lncRNAs: NR_002704, ENSRNOT00000062543, and Zfas1. Thus, our study demonstrated differential expression of a series of lncRNAs in the rat hippocampus after TBI, which may be correlated with post-TBI physiological and pathological processes. The findings also may provide novel targets for further investigation of both the molecular mechanisms underlying TBI and potential therapeutic interventions.