Articles: traumatic-brain-injuries.
-
Acute kidney injury (AKI), a prevalent non-neurological complication following traumatic brain injury (TBI), is a major clinical issue with an unfavorable prognosis. This study aimed to develop and validate machine learning models to predict severe AKI (stage 3 or greater) incidence in patients with TBI. ⋯ In this study, the RF model demonstrated better discrimination in predicting severe AKI than other models. An online calculator could facilitate its application, potentially improving the early detection of severe AKI and subsequently improving the clinical outcomes among patients with msTBI.
-
Invasive neuromonitoring has become an important part of pediatric neurocritical care, as neuromonitoring devices provide objective data that can guide patient management in real time. New modalities continue to emerge, allowing clinicians to integrate data that reflect different aspects of cerebral function to optimize patient management. Currently, available common invasive neuromonitoring devices that have been studied in the pediatric population include the intracranial pressure monitor, brain tissue oxygenation monitor, jugular venous oximetry, cerebral microdialysis, and thermal diffusion flowmetry. In this review, we describe these neuromonitoring technologies, including their mechanisms of function, indications for use, advantages and disadvantages, and efficacy, in pediatric neurocritical care settings with respect to patient outcomes.
-
Journal of neurotrauma · Apr 2023
Therapeutic role of microRNAs of small extracellular vesicles from human mesenchymal stromal/stem cells in the treatment of experimental traumatic brain injury.
Mesenchymal stem/stromal cells (MSC)-derived small extracellular vesicles (sEVs) possess therapeutic potential for treatment of traumatic brain injury (TBI). The essential role of micro ribonucleic acids (miRNAs) underlying the beneficial effects of MSC-derived sEVs for treatment of TBI remains elusive. The present study was designed to investigate the role of microRNAs in sEVs from MSCs with Argonaute 2 knockdown (Ago2-KD) in neurological recovery, neuroinflammation, and neurovascular remodeling in TBI rats. ⋯ The therapeutic effects of Ago2-KD-sEV were comparable to that of vehicle treatment. Our findings demonstrate that attenuation of Ago2 protein in MSCs reduces miRNAs in MSC-derived sEVs and abolishes exosome treatment-induced beneficial effects in TBI recovery, suggesting that miRNAs in MSC-derived sEVs play an essential role in reducing neuronal cell loss, inhibiting neuroinflammation, and augmenting angiogenesis and neurogenesis, as well as improving functional recovery in TBI. The findings underscore the important role of miRNAs in MSC-derived sEVs in the treatment of TBI.
-
Emerg Med Australas · Apr 2023
Observational StudyIncidence of traumatic brain injuries in head-injured children with seizures.
Incidence and short-term outcomes of clinically important traumatic brain injury (ciTBI) in head-injured children presenting to ED with post-traumatic seizure (PTS) is not described in current literature. ⋯ PTS was uncommon in head-injured children presenting to the ED but associated with an increased risk of ciTBI in those with reduced GCS on arrival.
-
Journal of neurotrauma · Apr 2023
Innate and peripheral immune alterations after TBI are regulated in a gut microbiota-dependent manner in mice.
Traumatic brain injury (TBI) patients are at high risk for disruption of the gut microbiome. Previously, we have demonstrated that broad-spectrum antibiotic exposure after TBI drastically alters the gut microbiota and modulates neuroinflammation, neurogenesis, and long-term fear memory. However, these data did not determine if the impact of antibiotic exposure on the brain's response to injury was mediated directly by antibiotics or indirectly via modulation of the gut microbiota. ⋯ At 7 days post-injury, GF-VNAM had increased microglial activation, reduced infiltration of T cells, and decreased neurogenesis. Similarly, SPF mice exposed to antibiotics prior to but not after injury demonstrated similar alterations in neuroinflammation and neurogenesis compared with control mice. These data support our hypothesis implicating the gut microbiota as an important modulator of the neuroinflammatory process and neurogenesis after TBI and provide an exciting new approach for neuroprotective therapeutics for TBI.