BACKGROUND: Nonconvulsive seizures are a major source of in-hospital morbidity and a cause of unexplained encephalopathy in critically ill patients. Electroencephalography (EEG) is essential to confirm nonconvulsive seizures and can guide patient-specific workup, treatment, and prognostication. In a 208-bed community hospital, EEG services were limited to 1 part-time EEG technician and 1 EEG machine shared between inpatient and outpatient settings.
View Article and Find Full Text PDFA variety of in vitro models have been developed to understand the mechanisms underlying the regenerative failure of central nervous system (CNS) axons, and to guide pre-clinical development of regeneration-promoting therapeutics. These range from single-cell based assays that typically focus on molecular mechanisms to organotypic assays that aim to recapitulate in vivo behavior. By utilizing a combination of models, researchers can balance the speed, convenience, and mechanistic resolution of simpler models with the biological relevance of more complex models.
View Article and Find Full Text PDFAstrocyte phenotypes change in a process called reactive gliosis after traumatic central nervous system (CNS) injury. Astrogliosis is characterized by expansion of the glial fibrillary acidic protein (GFAP) cytoskeleton, adoption of stellate morphologies, and differential expression of some extracellular matrix molecules. The astrocytic response immediately after injury is beneficial, but in the chronic injury phase, reactive astrocytes produce inhibitory factors (i.
View Article and Find Full Text PDFObject: Simultaneous traumatic brain injury (TBI) and aortic injury has been considered unsurvivable for many years because treatments such as sedation and blood pressure goals conflict for these 2 conditions. Additionally, surgical interventions for aortic injury often require full anticoagulation, which is contraindicated in patients with TBI. For these reasons, and due to the relative rarity of aortic injury/TBI, little data are available to guide treating physicians.
View Article and Find Full Text PDFInjured retinal ganglion cell (RGC) axons do not regenerate spontaneously, causing loss of vision in glaucoma and after trauma. Recent studies have identified several strategies that induce long distance regeneration in the optic nerve. Thus, a pressing question now is whether regenerating RGC axons can find their appropriate targets.
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