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Dataset results
993 results for “Traumatic Brain Injury”
Study to Evaluate the Safety, Tolerability, and Efficacy of Armodafinil as Treatment for Patients With Excessive Sleepiness Associated With Mild or Moderate Closed Traumatic Brain Injury
ClinicalTrials.gov study NCT00983437. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Treatment of Post-Traumatic Brain Injury (TBI) Depression
ClinicalTrials.gov study NCT00233103. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Efficacy of Xeomin for Migraines in Patients With Traumatic Brain Injuries vs. Anomalous Health Incidents
ClinicalTrials.gov study NCT07267819. IPD Sharing: NO. Countries: 1. Publications: 16.
Treatment Strategy to Prevent Mood Disorders Following Traumatic Brain Injury
ClinicalTrials.gov study NCT00704379. IPD Sharing: Not stated. Countries: 1. Publications: 29.
Hypertonic Resuscitation Following Severe Traumatic Brain Injury (TBI)
ClinicalTrials.gov study NCT00316004. IPD Sharing: Not stated. Countries: 2. Publications: 2.
Treating Civilian Traumatic Brain Injury With High Definition Transcranial Direct Current Stimulation (ciTBI-HDtDCS)
ClinicalTrials.gov study NCT05408975. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.
Neurofeedback-enhanced Mindfulness Meditation in Traumatic Brain Injury
ClinicalTrials.gov study NCT02615535. IPD Sharing: YES. Countries: 1. Publications: 5.
Prioritization of Cerebral Deoxygenation in Severe Traumatic Brain Injury and Mortality Benefit.
ClinicalTrials.gov study NCT06306950. IPD Sharing: NO. Countries: 1. Publications: 7.
Assessment of Dystussia in Traumatic Brain Injury
ClinicalTrials.gov study NCT02240329. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Anger Self-Management in Traumatic Brain Injury
ClinicalTrials.gov study NCT01745146. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Top-Down Executive Control in Traumatic Brain Injury (TBI), PTSD and Combined
ClinicalTrials.gov study NCT01072006. IPD Sharing: NO. Countries: 1. Publications: 1.
Data from: Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
Open the record for dataset details and reuse information.
Data from: Sociosexual and communication deficits after traumatic injury to the developing murine brain
Despite the life-long implications of social and communication dysfunction after pediatric traumatic brain injury, there is a poor understanding of these deficits in terms of their developmental trajectory and underlying mechanisms. In a well-characterized murine model of pediatric brain injury, we recently demonstrated that pronounced deficits in social interactions emerge across maturation to adulthood after injury at postnatal day (p) 21, approximating a toddler-aged child. Extending these findings, we here hypothesized that these social deficits are dependent upon brain maturation at the time of injury, and coincide with abnormal sociosexual behaviors and communication. Age-dependent vulnerability of the developing brain to social deficits was addressed by comparing behavioral and neuroanatomical outcomes in mice injured at either a pediatric age (p21) or during adolescence (p35). Sociosexual behaviors including social investigation and mounting were evaluated in a resident-intruder paradigm at adulthood. These outcomes were complemented by assays of urine scent marking and ultrasonic vocalizations as indices of social communication. We provide evidence of sociosexual deficits after brain injury at p21, which manifest as reduced mounting behavior and scent marking towards an unfamiliar female at adulthood. In contrast, with the exception of the loss of social recognition in a three-chamber social approach task, mice that received TBI at adolescence were remarkably resilient to social deficits at adulthood. Increased emission of ultrasonic vocalizations (USVs) as well as preferential emission of high frequency USVs after injury was dependent upon both the stimulus and prior social experience. Contrary to the hypothesis that changes in white matter volume may underlie social dysfunction, injury at both p21 and p35 resulted in a similar degree of atrophy of the corpus callosum by adulthood. However, loss of hippocampal tissue was greater after p21 compared to p35 injury, suggesting that a longer period of lesion progression or differences in the kinetics of secondary pathogenesis after p21 injury may contribute to observed behavioral differences. Together, these findings indicate vulnerability of the developing brain to social dysfunction, and suggest that a younger age-at-insult results in poorer social and sociosexual outcomes.
Effectiveness of Mannitol Use on Clinical Outcomes of Severe Traumatic Brain Injury Patients
<p>Data set for article entitled: </p> <p><span>Effectiveness of Mannitol Use on Clinical Outcomes of Severe Traumatic Brain Injury Patients</span></p>
Data from: Age-at-injury influences the glial response to traumatic brain injury in the cortex of male juvenile rats
<p>Glia influence neuronal development and aging. Few translational studies have examined how age at injury affects the glial response to traumatic brain injury (TBI). We hypothesized that rats injured before sexual maturity would exhibit a greater glial response, that persists into early adulthood, compared to rats injured near the onset of sexual maturity.</p> <p>Postnatal day (PND)17 and PND35 rats received midline fluid percussion injury or sham surgery. In three cortical regions (peri-injury, S1BF, perirhinal), we investigated the glial response relative to age at injury, time post-injury (2H, 1D 7D, 25D, and 43D), and post-natal age, such that rats injured at PND17 or PND35 were compared at the same post-natal-age (e.g., PND17+25d post-injury=PND42; PND35+7d post-injury=PND42). We measured Iba1+ microglia cells and quantified their activation status. GFAP expression was examined using immunohistochemistry. Data were analyzed using Bayesian multivariate multi-level models.</p> <p>Independent of age at injury, TBI activated microglia (shorter branches, fewer endpoints) in the cortex with more microglia in all regions compared to shams. TBI-induced microglial activation was sustained in the S1BF into early adulthood (PND60). PND17 injured rats had more microglial activation in the perirhinal cortex than PND35 injured rats. Activation was not confounded by age-dependent cell size changes, and microglial cell body sizes were similar between ages.</p> <p>Increased microglial activation in PND17 injured rats suggests that TBI upregulates the glial response at discrete stages of development. Age at injury and aging with an injury are translationally important because experiencing a TBI during early childhood may trigger an exaggerated glial response.</p>
Effectiveness of Mannitol Use on Clinical Outcomes of Severe Traumatic Brain Injury Patients
<p>Dataset for article entitled: </p> <p><span>Effectiveness of Mannitol Use on Clinical Outcomes of Severe Traumatic Brain Injury Patients</span></p>
Time Dependent Analysis of Rat Microglial Markers in Traumatic Brain Injury Reveals Dynamics of Distinct Cell Subpopulations
<p>The repository contains seven zip files for flow cytometry data for rat microglia following Controlled cortical impact (CCI) collected at seven time points: 3 hours, 1 day, 2 days, 7 days 14 days, 21 days and 28 days.</p> <p>Each file contains 24 CSV files converted from the raw fcs file and text files that contain meta data about the file.</p> <p>Each file name depicts the information of whether it is Panel A (M1 in the file name) or Panel B (M2 in the file name) measurement and whether the measurement was conducted on the ipsilateral (ipsi) or contralateral (contra) side of the CCI, or sham conducted on the ipsilateral (ipsi) or contralateral (contra) sides.</p> <p>Below is the description of the columns of each file:</p> <table> <tbody> <tr> <td> <p><strong>File column name</strong></p> </td> <td> <p><strong>Original name</strong></p> </td> <td> <p><strong>Panel A (M1) context</strong></p> </td> <td> <p><strong>PAnel B (M2) context</strong></p> </td> <td> <p><strong>Description</strong></p> </td> </tr> <tr> <td> <p>F0</p> </td> <td> <p>FSC-A</p> </td> <td> <p>FSC-A</p> </td> <td> <p>FSC-A</p> </td> <td> <p>Forward scattering Area</p> </td> </tr> <tr> <td> <p>F1</p> </td> <td> <p>FSC-H</p> </td> <td> <p>FSC-H</p> </td> <td> <p>FSC-H</p> </td> <td> <p>Forward scattering Height</p> </td> </tr> <tr> <td> <p>F2</p> </td> <td> <p>FSC-W</p> </td> <td> <p>FSC-W</p> </td> <td> <p>FSC-W</p> </td> <td> <p>Forward scattering Width</p> </td> </tr> <tr> <td> <p>F3</p> </td> <td> <p>SSC-A</p> </td> <td> <p>SSC-A</p> </td> <td> <p>SSC-A</p> </td> <td> <p>Side scattering area</p> </td> </tr> <tr> <td> <p>F4</p> </td> <td> <p>FITC-A</p> </td> <td> <p>FITC-A</p> </td> <td> <p>FITC-A</p> </td> <td> <p>Fluorescein isothiocyanate</p> </td> </tr> <tr> <td> <p>F5</p> </td> <td> <p>PE-A</p> </td> <td> <p>CD32</p> </td> <td> <p>CD200R</p> </td> <td> <p>Protein expression</p> </td> </tr> <tr> <td> <p>F6</p> </td> <td> <p>PerCP-Cy5-5-A</p> </td> <td> <p>-</p> </td> <td> <p>CD163</p> </td> <td> <p>Protein expression</p> </td> </tr> <tr> <td> <p>F7</p> </td> <td> <p>PE-Cy7-A</p> </td> <td> <p>CD11</p> </td> <td> <p>CD11</p> </td> <td> <p>Protein expression</p> </td> </tr> <tr> <td> <p>F8</p> </td> <td> <p>BV421-A</p> </td> <td> <p>P2Y12</p> </td> <td> <p>P2Y12</p> </td> <td> <p>Protein expression</p> </td> </tr> <tr> <td> <p>F9</p> </td> <td> <p>BV510-A</p> </td> <td> <p>-</p> </td> <td> <p>-</p> </td> <td> <p>Dye </p> </td> </tr> <tr> <td> <p>F10</p> </td> <td> <p>Alexa Fluor 647-A</p> </td> <td> <p>CD86</p> </td> <td> <p>RT1B</p> </td> <td> <p>Protein expression</p> </td> </tr> <tr> <td> <p>F11</p> </td> <td> <p>APC-Cy7-A</p> </td> <td> <p>CD45</p> </td> <td> <p>CD45</p> </td> <td> <p>Protein expression</p> </td> </tr> <tr> <td> <p>F12</p> </td> <td> <p>Event Time</p> </td> <td> <p>Event Time</p> </td> <td> <p>Event Time</p> </td> <td>Event Time</td> </tr> </tbody> </table>
Master data of the article "Effect of ethanol extract of nigella sativa L seeds and propofol on BDNF protein level as neuroplasticity and neuroprotection of traumatic brain injury in rats"
<p><strong>Master data of the article "Effect of ethanol extract of nigella sativa L seeds and propofol on BDNF protein level as neuroplasticity and neuroprotection of traumatic brain injury in rats"</strong></p>
Deployment Related Mild Traumatic Brain Injury (mTBI)
ClinicalTrials.gov study NCT01847040. IPD Sharing: Not stated. Countries: 1. Publications: 6.
An Observational Exploration of Clinical Trials Targeting Traumatic Brain Injury
ClinicalTrials.gov study NCT06264518. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
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.