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993 results for “Traumatic brain injury”
The language network reemerges during recovery from severe traumatic brain injury
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Genome- and transcriptome-wide association summary statistics for outcome from traumatic brain injury
<p>The dataset contains summary statistics for the genome- and transcriptome-wide association studies (GWAS, TWAS) of genetic effects on outcome in traumatic brain injury (TBI). The study participants attended hospital within 24 hours of TBI, and underwent head computed tomography imaging.</p> <p><strong>Study participants</strong></p> <p>European ancestry data set contains 4710 individuals; multi-ethnic cohort 5268 individuals, including Europeans (n = 4710), Africans (n = 245) and Admixed Americans (n = 313).</p> <p>The largest European population contribution was from CENTER-TBI (Collaborative European NeuroTrauma Effectiveness Research, https://www.center-tbi.eu), where each participating center (60 centers from 20 countries in Europe) recruited patients between December 2013 and December 2017. The patients recruited in CENTER-TBI were supplemented by subjects from cohorts recruited at two European centres (Cambridge, UK, and Turku, Finland).</p> <p>The majority of patients in the US cohort were recruited between 2014 and 2018 to TRACK-TBI (Transforming Research and Clinical Knowledge in TBI, https://tracktbi.ucsf.edu) by the 18 US participant sites. The subjects recruited to the US cohort from TRACK-TBI were supplemented by patients recruited to an institutional research initiative at Mass General Brigham (MGB).</p> <p><strong>Outcome definition</strong></p> <p>Outcomes were measured using the extended Glasgow Outcome Scale (GOSE), ranging from 1 (dead) to 8 (upper good recovery), measured 6 months post-TBI. TBI severity was specified using the Glasgow Coma Score (GCS), with TBI classified as mild (GCS 13-15), moderate (GCS 9-12), or severe (GCS 3-8).</p> <p>To account for the effect of injury severity on outcome, sliding dichotomization was used to categorize outcome as favourable or unfavourable. A GOSE ≤ 4 was used to define an unfavourable outcome for patients with either moderate (GCS 9-12) or severe (GCS 3-8) TBI, while the unfavourable group was extended to patients with GOSE ≤ 7 if they had mild (GCS 13-15) TBI.</p> <p><strong>Genotype data and imputation</strong></p> <p>Genotyping was completed at FIMM Technology Center for CENTER-TBI, Cambridge, Turku patients and the Broad Institute for TRACK-TBI, using the Illumina Global Screening Array (GSA-24v2-0 + Multi-Disease). The MGB cohort were genotyped using Illumina’s Multi-Ethnic Global array (MEGA) and the pre-releases forms, including MEGA and MEGA-Ex arrays at Illumina at the MGB Translational Genomics Core.</p> <p>A unified quality control procedure was applied for each study cohort and the array-based genotypes were imputed using the Haplotype Reference Consortium panel. Autosomal chromosomes were considered, post-imputation data was filtered by imputation quality (INFO > 0.4 for CENTER-TBI, Cambridge and Turku; R2 > 0.4 for TRACK-TBI and MGB) and MAF > 1%.</p> <p><strong>Genome-wide association analysis and meta-analysis</strong></p> <p>Genome-wide single-marker scans were performed using a penalized likelihood-based Firth logistic regression, and implemented in PLINK v2.0. Using favourable outcome as reference, models were fitted on the basis of imputed allelic dosages. Age, sex, major extracranial injury, pupillary reactivity, and the first 10 principal components were included as covariates. Study cohort (CENTER-TBI, Cambridge, Turku) was an additional covariate in the CENTER-TBI GWAS.</p> <p>Fixed-effects meta-analysis of the three European ancestry GWAS was performed using METAL. For trans-ethnic meta-analysis, summary statistics of five GWASs in patients of European, African and Admixed Americans were aggregated via MR-MEGA.</p> <p><strong>Transcriptome-wide association study</strong></p> <p>Genetically regulated gene expression (GREx) was imputed using a regression model fitted on a separate gene expression database. Elastic net models provided by PrediXcan for all available GTEx brain tissues and whole blood were used. For TWAS, the same sliding dichotomy model for outcome with the same set of covariates as in the GWAS, but PCA components were replaced with the top five principal components of the respective gene expression data. </p> <p><strong>Column headers - GWAS</strong></p> <p>rsID: variant rsID<br> Chrom: chromosome<br> Pos: position (build GRCh38)<br> A1: effect allele<br> A2: reference allele<br> EAF: allele frequency of effect allele<br> Effect: effect size of effect allele<br> StdErr: standard error of effect size<br> P: p value of association (with genomic correction)<br> N: sample size</p> <p>Note. 'Effect' and 'StdErr' are only available for the European ancestry meta-analysis.</p> <p><br> <strong>Column headers - TWAS</strong></p> <p>tissue: GTEx tissue type<br> id: ensembl gene id<br> coef: model coefficient<br> se: model standard error for coefficient<br> p: model-based p value<br> symbol: gene symbol<br> name: gene name written out<br> chr: chromosome<br> start: gene start position (build GRCh38)</p>
Epidemiological and clinical characteristics predictive of ICU mortality of traumatic brain injury patients treated at a trauma reference hospital – A cohort study - Dataset
<p><strong>Dataset of a cohort whose summary is described below.</strong></p> <p><strong>ABSTRACT</strong></p> <p><strong>Background</strong>: Traumatic brain injury (TBI) has substantial physical, psychological, social and economic impacts, with high rates of morbidity and mortality. Considering its high incidence, the aim of this study was to identify epidemiological and clinical characteristics that predict mortality in patients hospitalized for TBI in intensive care units (ICUs). <strong>Methods</strong>: A retrospective cohort study was carried out with patients over 18 years old with TBI admitted to an ICU of a Brazilian trauma referral hospital between January 2012 and August 2019. TBI was compared with other traumas in terms of clinical characteristics of ICU admission and outcome. Univariate and multivariate analyses were used to estimate the odds ratio for mortality. <strong>Results</strong>: Of the 4816 patients included, 1114 had TBI, with a predominance of males (85.1%). Compared with patients with other traumas, patients with TBI had a lower mean age (45.3 ± 19.1 versus 57.1 ± 24.1 years, p < 0.001), higher median APACHE II (19 versus 15, p <0.001) and SOFA (6 versus 3, p < 0.001) scores, lower median Glasgow Coma Scale (GCS) score (10 versus 15, p < 0.001), higher median length of stay (7 days versus 4 days, p < 0.001) and higher mortality (27.6% versus 13.3%, p < 0.001). In the multivariate analysis, the predictors of mortality were older age (OR: 1.008 [1.002-1.015], p = 0.016), higher APACHE II score (OR: 1.180 [1.155-1.204], p < 0.001), lower GCS score for the first 24 hours (OR: 0.730 [0.700-0.760], p < 0.001), and greater number of brain injuries and presence of associated chest trauma (OR: 1.727 [1.192-2.501], p < 0.001). <strong>Conclusion</strong>: Patients admitted to the ICU for TBI were younger and had worse prognostic scores, longer hospital stays and higher mortality than those admitted to the ICU for other traumas. The independent predictors of mortality were advanced age, APACHE II score, first 24-hour GCS score, number of brain injuries and chest trauma.</p>
Improving Outcomes for Care Partners of Persons With Traumatic Brain Injury
ClinicalTrials.gov study NCT04570930. IPD Sharing: YES. Countries: 1. Publications: 2.
Sleep Management And Recovery After Traumatic Brain Injury in Kids: Pilot Intervention of Melatonin
ClinicalTrials.gov study NCT04932096. IPD Sharing: YES. Countries: 1. Publications: 3.
Effectiveness of Mannitol Use on Clinical Outcomes of Severe Traumatic Brain Injury Patients
<p>Dataset for manuscript entitled: </p> <p><span>Effectiveness of Mannitol Use on Clinical Outcomes of Severe Traumatic Brain Injury Patients</span></p>
Supplementary materials of Brain Extract of Subacute Traumatic Brain Injury Promotes Neuronal Differentiation of Human Neural Stem Cells Via Autophagy
<p>Figure S1: Characterization of hNSCs. In proliferate medium, the embryo derived hNSCs could form the neurospheres (A). Markers of NSCs (NES, SOX2, SOX1) were detected (B). The SOX2<sup>+</sup> cells accounted for >95% of all cells (C). Bar scale: 60μm;</p> <p>Figure S2: The proliferation of hNSCs in TBI brain extracts with different phases. Differentiated hNSCs could be labeled with EdU in TBI brain extracts with different phases (A). Ratio of EdU<sup>+</sup> cells was decreased with the progression of days post-injury (B). Bar scale: 75μm; ****: P<0.0001;</p> <p>Figure S3: The GO annotations and KEGG pathway analysis of different expressed pro-teins in acute brain extract and subacute brain extract;</p> <p>Table S1: The protein profiles of brain extract in acute phase and subacute phase after TBI.</p>
Data from: Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
<p><span>Cognitive impairments are a common consequence of traumatic brain injury (TBI). The hippocampus is a subcortical structure that plays a key role in the formation of declarative memories and is highly vulnerable to TBI. The α7 nicotinic acetylcholine receptor (nAChR) is highly expressed in the hippocampus and reduced expression and function of this receptor are linked with cognitive impairments in Alzheimer's disease and schizophrenia. Positive allosteric modulation of α7 nAChRs with AVL-3288 enhances receptor currents and improves cognitive functioning in naïve animals and healthy human subjects. Therefore, we hypothesized that targeting the α7 nAChR with the positive allosteric modulator AVL-3288 would enhance cognitive functioning in the chronic recovery period of TBI. To test this hypothesis, adult male Sprague Dawley rats received moderate parasagittal fluid-percussion brain injury or sham surgery. At 3 months after recovery, animals were treated with vehicle or AVL-3288 at 30 min prior to cue and contextual fear conditioning and the water maze task. Treatment of TBI animals with AVL-3288 rescued learning and memory deficits in water maze retention and working memory. AVL-3288 treatment also improved cue and contextual fear memory when tested at 24 hr and 1 month after training, when TBI animals were treated acutely just during fear conditioning at 3 months post-TBI. Hippocampal atrophy but not cortical atrophy was reduced with AVL-3288 treatment in the chronic recovery phase of TBI. AVL-3288 application to acute hippocampal slices from animals at 3 months after TBI rescued basal synaptic transmission deficits and long-term potentiation (LTP) in area CA1. Our results demonstrate that AVL-3288 improves hippocampal synaptic plasticity, and learning and memory performance after TBI in the chronic recovery period. Enhancing cholinergic transmission through positive allosteric modulation of the α7 nAChR may be a novel therapeutic to improve cognition after TBI.</span></p>
Dataset related to article "Systematic review and meta-analysis of preclinical studies testing mesenchymal stromal cells for traumatic brain injury"
<p>Mesenchymal stromal cells (MSCs) are widely used in preclinical models of traumatic brain injury (TBI). Results are promising in terms of neurological improvement but are hampered by wide variability in treatment responses. We made a systematic review and meta-analysis: 1) to assess the quality of evidence for MSC treatment in TBI rodent models; 2) to determine the effect size of MSCs on sensorimotor function, cognitive function and anatomical damage; 3) to identify MSC-related and protocol-related variables associated with greater efficacy; 4) to understand whether MSC manipulations boost therapeutic efficacy.</p> <p>The meta-analysis included 80 studies. After TBI, MSCs improved sensorimotor and cognitive deficits, and reduced anatomical damage. Stratified meta-analysis on sensorimotor outcome showed similar efficacy for different MSC sources and for syngeneic or xenogenic transplants. Efficacy was greater when MSCs were delivered in the first week post-injury, and when implanted directly into the lesion cavity. The greatest effect size was for cells embedded in matrices or for MSC-derivatives.</p> <p>MSC therapy is effective in preclinical TBI models, improving sensorimotor, cognitive and anatomical outcomes, with large effect sizes. These findings support clinical studies in TBI.</p> <p>The present dataset reports extrapolated data used for the meta-analysis</p>
Neuromodulation and Yoga for Mild Traumatic Brain Injury and Chronic Pain
ClinicalTrials.gov study NCT04517604. IPD Sharing: YES. Countries: 1. Publications: 1.
Deep Brain Stimulation for the Treatment of Traumatic Brain Injury
ClinicalTrials.gov study NCT02881151. IPD Sharing: NO. Countries: 1. Publications: 2.
Evaluation, Pathogenesis, and Outcome of Subjects With or Suspected Traumatic Brain Injury
ClinicalTrials.gov study NCT01132937. IPD Sharing: UNDECIDED. Countries: 1. Publications: 5.
Traumatic Brain Injury (TBI) Screening Instruments
ClinicalTrials.gov study NCT00875329. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Light Therapy for Moderate Traumatic Brain Injury
ClinicalTrials.gov study NCT02233413. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Effects of Bright Light Therapy in Mild Traumatic Brain Injury
ClinicalTrials.gov study NCT01747811. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Efficacy and Safety Study of Intravenous Progesterone in Patients With Severe Traumatic Brain Injury
ClinicalTrials.gov study NCT01143064. IPD Sharing: Not stated. Countries: 21. Publications: 3.
Hyperbaric Oxygen Therapy (HBO2) for Persistent Post-concussive Symptoms After Mild Traumatic Brain Injury (mTBI)
ClinicalTrials.gov study NCT01306968. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Neuroendocrine Dysfunction in Traumatic Brain Injury: Effects of Testosterone Therapy
ClinicalTrials.gov study NCT01201863. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Window to Hope-Evaluating a Psychological Treatment for Hopelessness Among Veterans With Traumatic Brain Injury
ClinicalTrials.gov study NCT01691378. IPD Sharing: NO. Countries: 1. Publications: 2.
Study of Airway Pressure Release Ventilation and Intracranial Pressure in Patients With Severe Traumatic Brain Injury
ClinicalTrials.gov study NCT02507973. IPD Sharing: NO. Countries: 1. Publications: 22.
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.