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Traumatic brain injury (TBI) is a global public health problem, causing long-term burden to patients and caregivers. Patients and their families often resort to seeking online information regarding TBI management while awaiting formal health care consultations. Although this information is accessible and immediately available, little is known about the quality of online resources. We evaluated the accessibility, relevance, and readability of information regarding TBI from major online search engines. TBI-related search terms were entered into 2 online search engines (Google and Yahoo), and the first 30 websites per search were assessed for eligibility. Quality (DISCERN score, JAMA Benchmark score) and readability (Flesch–Kincaid Grade Level, Flesch Reading Ease Score) were assessed. Associations between search ranking, quality, and readability were evaluated. In total, 202 websites were evaluated with mean DISCERN score 36.5 ± 9.9/80, signifying poor global quality, and mean JAMA Benchmark score 2.8 ± 1.1/4. The majority required 9–12 years of education (113/202; 55.9%) according to Flesch–Kincaid Grade Level and categorized as "Difficult" on Flesch Reading Ease Score (94/202; 46.5%). Website quality was not associated with search ranking or readability. There is a paucity of high-quality online resources for patients with TBI. Herein, we highlight: 1) the importance of guidance from healthcare professionals regarding online-information seeking; and 2) recommendations for the most useful online resources available. [ABSTRACT FROM AUTHOR]

Despite medical advances, neurological recovery after severe traumatic brain injury (TBI) remains poor. Elevated levels of high mobility group box protein-1 (HMGB1) are associated with poor outcomes; likely via interaction with receptors for advanced-glycation-end-products (RAGE). We examined the hypothesis that HMGB1 post-TBI is anti-neurogenic and whether this is pharmacologically reversible. Post-natal rat cortical mixed neuro-glial cell cultures were subjected to needle-scratch injury and examined for HMGB1-activation/neuroinflammation. HMGB1-related genes/networks were examined using genome-wide RNA-seq studies in cortical perilesional tissue samples from adult mice. Post-natal rat cortical neural stem/progenitor cell cultures were generated to quantify effects of injury-condition medium (ICM) on neurogenesis with/without RAGE antagonist glycyrrhizin. Needle-injury upregulated TNF-α/NOS-2 mRNA-expressions at 6 h, increased proportions of activated microglia, and caused neuronal loss at 24 h. Transcriptome analysis revealed activation of HMGB1 pathway genes/canonical pathways in vivo at 24 h. A 50% increase in HMGB1 protein expression, and nuclear-to-cytoplasmic translocation of HMGB1 in neurons and microglia at 24 h post-injury was demonstrated in vitro. ICM reduced total numbers/proportions of neuronal cells, but reversed by 0.5 μM glycyrrhizin. HMGB1 is activated following in vivo post mechanical injury, and glycyrrhizin alleviates detrimental effects of ICM on cortical neurogenesis. Our findings highlight glycyrrhizin as a potential therapeutic agent post-TBI. [ABSTRACT FROM AUTHOR]