DATASET CITATION:
Norris C., Murphy S. F., VandeVord P. J., Weatherbee J. (2024) Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury in male Sprague Dawley rats. Open Data Commons for Traumatic Brain Injury. ODC-TBI:1014 http://dx.doi.org/10.34945/F5BP43
ABSTRACT:
STUDY PURPOSE: The purpose of this study was to optimize and validate methods measuring brain metabolite concentrations in naïve male Sprague Dawley rats and then utilize these methods to detect changes in regional metabolite concentrations at 4 hours following blast exposure.
DATA COLLECTED: Data was collected using high performance liquid chromatography (HPLC) with electrochemical detection. Methods were optimized to quantify alanine, arginine, aspartate, serine, taurine, threonine, tyrosine, glycine, glutamate, glutamine, and gamma-Aminobutyric acid (GABA) in the serum, cerebrospinal fluid, hippocampus, cortex, and cerebellum of 10 week old naïve male Sprague Dawley rats (n = 6). A subsequent preliminary study was performed investigating acute changes in free amino acid concentrations following blast-induced traumatic brain injury (bTBI). Rats were exposed to a single head-on blast wave averaging 126 kPa using an Advanced Blast Simulator. HPLC analytic methods were employed to statistically compare changes in sham (n = 4) and blast (n = 4) concentrations of these metabolites at 4 hours post-injury in the hippocampus and cortex regions.
CONCLUSIONS: Molecular precursors (alanine, arginine, serine, glutamine) decreased in concentration on average by about 10-15% at 4 hours following blast exposure in both the cortex and hippocampus while neurotransmitter concentrations (glycine, taurine, aspartate, glutamate, GABA) remained unchanged relative to the sham group.
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DATASET CITATION:
Rowe R. K., Green T. R F., Murphy S. M. (2023) Quantification of extravasated blood in the brain and microglial morphologies following midline fluid percussion in male juvenile rats. Open Data Commons for Traumatic Brain Injury. ODC-TBI:874 http://dx.doi.org/10.34945/F5Q304
ABSTRACT:
STUDY PURPOSE: We hypothesized that blood brain barrier (BBB) dysfunction positively predicts microglial activation and that vulnerability to BBB dysfunction and associated neuroinflammation are dependent on age-at-injury.
DATA COLLECTED: Post-natal-day (PND)17 and PND35 rats (n = 56) received midline fluid percussion injury or sham surgery. At pre-determined time points post-injury (1, 7, and 25 days), brains were collected and cryosectioned coronally at 40 µm. Immunoglobulin-G (IgG) stain was quantified as a marker of extravasated blood in the brain and BBB dysfunction. For IgG staining, slides were washed in PBS then incubated in a blocking solution (10% normal goat serum [NGS], 1% triton X-100 in PBS) for 120 minutes. Blocking solution was removed and antibody solution (biotinylated anti-rat IgG [H + L] at 1:250 concentration in 1% NGS and PBS) was applied to each slide and left to incubate at room temperature for 60 minutes. Slides were washed in PBS. Endogenous peroxidases were blocked for 30 minutes. After washing in PBS, ABC solution was applied and incubated for 30 minutes. Slides were washed in PBS and DAB solution. IgG staining was analyzed under the microscope at successive magnifications of 5-40× to determine the presence or absence of bleeding in the following 7 areas: peri-injury cortex, primary somatosensory barrel field (S1BF) cortex, above the cornu ammonis (CA)3 region/beside the CA1 region/below the dentate gyrus of the hippocampus, hypothalamus, or other. These data were analyzed using a binary score to determine presence or absence of bleeding in the given areas and summed to give a cumulative score (minimum score 0, maximum score 7). A total of 80 µm was scored for each rat and averaged by investigators blinded to experimental conditions. For Iba-1 staining, slides were placed in sodium citrate buffer (pH 6.0) microwaved, then washed in PBS and incubated in blocking solution (4% normal horse serum [NHS], 0.1% Triton-100 in PBS) for 60 minutes. Slides were incubated in primary antibody solution (rabbit anti-Iba1; at 1:1000 concentration in 1% NHS, 0.1% triton-100 in PBS) overnight at 4 ºC. Slides were then washed in PBS + 0.1% tween-20. Secondary antibody solution (biotinylated horse anti-rabbit igG (H +L); vector BA-1100 at 1:250 concentration in 4% NHS and 0.4% triton-100 in PBS) was applied for 60 minutes. The tissue was then washed in PBS and endogenous peroxidases were blocked by placing slides in 200 ml PBS + 8 ml H2O2 for 30 minutes. After washing in PBS and 0.1% tween-20, ABC solution (Vectastain ABC kit PK-6100) was applied for 30 minutes. Slides were washed in PBS + 0.1% tween-20 and DAB solution (Vector DAB peroxidase substrate kit SK-4100) was applied to the slide for 10 minutes and immediately placed in water for 10 minutes. Slides were dehydrated by placing in successive concentrations (70%, 90%, 100% × 2) of ethanol. Tissue was placed in citrosolve and slides were cover slipped using DPX mounting medium. Z-stack images of Iba1 stained slides were taken. Images were analyzed using ImageJ and the skeletal analysis plugin. Microglial cell somas were counted and their areas and perimeters were measured. Images were converted to binary, skeletonized, and the analyze skeleton plugin was applied to measure the average number of branches, branch length, and number of endpoints per microglial cell captured in 40× photomicrographs. Total microglial count, process length, and endpoints were recorded and averaged per number of cells in each region of interest. The main objective of this study was to investigate BBB dysfunction and the microglial response in the hippocampus, hypothalamus, and motor cortex relative to age-at-injury and days post-injury (1, 7, 25). We measured the morphologies of Iba1-labeled microglia using cell body area and perimeter, microglial branch number and length, endpoints/microglial cell, and number of microglia. Data were analyzed using generalized hierarchical models.
CONCLUSIONS: In PND17 rats, TBI increased levels of IgG compared to shams. Independent of age-at-injury, IgG in TBI rats was higher at 1 and 7DPI but resolved by 25DPI, this was consistent in all regions. TBI activated microglia (more cells and fewer endpoints) in PND35 rats compared to respective shams. Independent of age-at-injury, TBI induced morphological changes indicative of microglial activation, which resolved by 25DPI in all regions. TBI rats had fewer cells and endpoints per cell at 1 and 7DPI than 25DPI in all regions. Independent of TBI, PND17 rats had larger, more activated microglia than PND35 rats; PND17 TBI rats had larger cell body areas and perimeters than PND35 TBI rats. Importantly, we found support in both ages that IgG quantification predicted microglial activation after TBI in all regions. The number of microglia increased with increasing IgG, whereas branch length decreased with increasing IgG, which together indicate microglial activation.
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DATASET CITATION:
Rowe R. K., Ortiz J., Murphy S. M. (2023) GH-axis disruption after TBI in male juvenile rats. Open Data Commons for Traumatic Brain Injury. ODC-TBI:823 http://dx.doi.org/10.34945/F5R30F
ABSTRACT:
STUDY PURPOSE: We have previously shown that specific to the pediatric population, children with a traumatic brain injury (TBI) diagnosis have 3.22 times the risk of a subsequent endocrine diagnosis compared with the general pediatric population, with the predominant endocrine disorder diagnoses of “precocious sexual development and puberty”, followed by, “pituitary dwarfism/growth hormone deficiencies”. We used these clinical observations to inform our translational research investigating growth hormone-axis disruption following diffuse TBI in the juvenile rat. In the current study, we used post-natal day 17 rats, which model early childhood in humans, and assessed body weights, plasma growth hormone levels, and mean number of somatostatin neurons at acute and chronic time points post-injury. We hypothesized that diffuse TBI in juvenile rats would alter circulating growth hormone levels due to damage to the hypothalamus, specifically somatostatin neurons.
DATA COLLECTED: Juvenile (post-natal day 17) male rats were subjected to midline fluid percussion injury or a control sham surgery. Following the injury, we measured the righting reflex time (time it took a rat to right itself). Body weights were collected prior to surgery/injury, post-operatively at 1, 2, and 3 days post-injury, then weekly until tissue was collected at pre-determined time points post-injury (1, 7, 18, 25, 43 days post-injury). At the terminal time point blood and brains were collected. Blood was centrifuged and plasma was isolated. Growth hormone levels were measured in plasma by ELISA. Brains were cryosectioned and stained to visualize somatostatin neurons in the hypothalamus. Three investigators blinded to the experimental conditions counted all stained neurons in 6-9 images per rat. Cell counts were tabulated using ImageJ software to manually label each cell using the ROI manager. These counts were averaged across sections per rat and across investigators to determine the mean number of somatostatin neurons per image per rat.
CONCLUSIONS: Diffuse traumatic brain injury suppressed acute neurological reflexes measured as a higher righting reflex time. Brain-injured rats had a lower terminal body weight at 18 days post-injury compared to shams. Growth hormone levels increased over time but were not significantly altered by brain injury. Brain-injured rats had fewer somatostatin neurons at 1 day post-injury compared to shams. The mean number of somatostatin neurons positively predicted the growth hormone levels independent of brain injury.
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DATASET CITATION:
Nielson J. L., Cooper S. R., Yue J. K., Sorani M. D., Inoue T., Yuh E. L., Lum P. Y., Carlsson G. E., Vassar M. J., Lingsma H. F., Gordon W. A., Valadka A. B., Okonkwo D. O., Manley G. T., Ferguson A. R. (2023) Imaging Features, Functional Recovery, and Selected Single Nucleotide Polymorphism Data from TRACK-TBI Pilot Dataset. Open Data Commons for Traumatic Brain Injury. ODC-TBI:954 http://dx.doi.org/10.34945/F5RW24
ABSTRACT:
STUDY PURPOSE: The goal of this specific analysis of a small set of TRACK-TBI Pilot dataset variables was to assess the role of specific genetic polymorphisms as biomarkers of patient outcome after mild TBI with analysis of 3 single nucleotide polymorphisms (SNPs) associated with altered striatal dopamine levels: ANKK1 C/T (rs1800497), COMT Met/Val (rs4680) and DRD2 C/T rs6277 genotypes.
DATA COLLECTED: This is a set of 586 de-identified adult human patients with mild traumatic brain injury (Glasgow Coma Score >12), from a dataset previously published as supplement by Nielson et al. 2017 (see originating publication and relevant links). Seventeen outcome measures were chosen based on clinical relevance, including computed tomography (CT) features, functional recovery (Glasgow Outcome Scale-Extended), cognitive outcomes (Wechsler Adult Intelligence Scale) and post-traumatic stress disorder (PTSD). CT features were derived acutely after brain injury. The functional, cognitive, and PTSD data were collected 6 months after injury.
CONCLUSIONS: Analysis identified a unique diagnostic subgroup of patients with unfavorable outcome after mild TBI that were significantly predicted by the presence of specific genetic polymorphisms.
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DATASET CITATION:
Johnson C. E. (2023) Open Field Blast (OFB) Data Gu Lab_2019_2020. Open Data Commons for Traumatic Brain Injury. ODC-TBI:882 http://dx.doi.org/10.34945/F5630G
ABSTRACT:
STUDY PURPOSE: Provide open-field low intensity blast (LIB) exposure for VA study. See relevant links for the related behaviour data
DATA COLLECTED: Time-Pressure data to determine: Blast-wave overpressure, overpressure duration, rise time, and impulse. Weather conditions at the blast time. See relevant links for the protocols
CONCLUSIONS: Subjects were exposed to low intensity blast exposure from an open field blast. Behavior and histology analysis was possible for all subjects post blast.
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DATASET CITATION:
Zuckerman A., Siedhoff H. R., Balderrama A., Cui J., Gu Z. (2023) Home-cage monitoring general behavior of C57BL/6J male mice during the CognitionWall test 3 months after open-field LIB exposure. Open Data Commons for Traumatic Brain Injury. ODC-TBI:872 http://dx.doi.org/10.34945/F59W23
ABSTRACT:
STUDY PURPOSE: Evaluate the chronic-phase behavioral alterations 3 months after exposure to low-intensity blast in a home-cage-like environment during the CognitionWall test.
DATA COLLECTED: A total of 52 male C57Bl/6J mice, 8 weeks old, were used. The mice were randomly allocated into one of two groups: Blast (n=29) or Sham (n=23). Mice in the Blast group were exposed to open-field low-pressure blast wave (46.6 kPa, maximum impulse of 60.0 kPa*ms), under anesthesia. Mice from the Sham group were anesthetized but were not exposed to the blast wave. 3 months post-exposure, general behavior on the locomotor activity of the mice was measured using the PhenoTyper® home-cages (Model 3000, Noldus Information Technology, The Netherlands) and CognitionWall™ system (Noldus Information Technology, The Netherlands). All mice were familiar with the home-cage environment by being placed in the PhenoTypers for three days before conducting the CognitionWall assessments. Each mouse was housed individually, and its activity was continuously measured for 96 hours at a sample rate of 15 fps. Program-acquired data were uploaded to the web-based AHCODA-DB (Sylics, Bilthoven, The Netherlands) for meta-analysis. Eighteen behavioral parameters were analyzed and included in this dataset. See protocols and other related data in the relevant links section below.
CONCLUSIONS: No significant differences were found between the Blast and Sham mice in different parameters of general behavior on the locomotor activity. These data provided the essential baseline of both LIB-exposed mice and Sham controls in order to exclude the possibility that different performances in the CognitionWall tasks were caused by differences in overall locomotor activity.
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DATASET CITATION:
Zuckerman A., Siedhoff H. R., Balderrama A., Cui J., Gu Z. (2023) Home-cage monitoring spontaneous activity of C57BL/6J male mice 3 months after open-field low-intensity blast exposure. Open Data Commons for Traumatic Brain Injury. ODC-TBI:871 http://dx.doi.org/10.34945/F5FK5C
ABSTRACT:
STUDY PURPOSE: Evaluate the chronic-phase behavioral alterations 3 months after exposure to low-intensity blast in a home-cage-like environment.
DATA COLLECTED: A total of 52 male C57Bl/6J mice, 8 weeks old, were used. The mice were randomly allocated into one of two groups: Blast (n=29) or Sham (n=23). Mice in the Blast group were exposed to open-field low-pressure blast wave (46.6 kPa, maximum impulse of 60.0 kPa*ms), under anesthesia. Mice from the Sham group were anesthetized but were not exposed to the blast wave. 3 months post-exposure, the spontaneous activity of the mice was measured using the PhenoTyper® home-cages (L = 30 × W = 30 × H = 35 cm; Model 3000, Noldus Information Technology, The Netherlands). Each mouse was housed individually, and its activity was continuously measured for 72 hours at a sample rate of 15 fps. Program-acquired data were uploaded to the web-based AHCODA-DB (Sylics, Bilthoven, The Netherlands) for meta-analysis. Twenty behavioral parameters were analyzed and included in this dataset. See protocols and other related data in the relevant links section below.
CONCLUSIONS: No significant differences were found between the Blast and Sham mice in different parameters of general daily performance behaviors, such as activity, arrests, and feeding zone visits.
Although no significant difference in long shelter visits between the Blast and Sham mice, was found, significant differences were found in multiple parameters of short shelter visits such as “shelter visit threshold” and “short shelter visit duration” (relevant to anxiety-like behaviors). Blast mice visited their shelters more frequently and for shorter periods of time than Sham mice in both dark and light phases. These results suggest that LIB-exposed mice may hold stable perceptions of environmental stimuli as a threat during activity bouts, whereas sham controls experienced such responses to a lesser degree. This type of performance is consistent as trait anxiety in humans, defined as a tendency to respond with concerns, troubles, and worries to non-threatening situations.
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DATASET CITATION:
Rowe R. K., Giordano K. R., Saber M., Green T. R.F.., Rojas-Valencia L. M., Ortiz J., Murphy S. M., Lifshitz J. (2022) Peripheral and central markers of inflammation after experimental brain injury in mice with depleted or intact microglia. Open Data Commons for Traumatic Brain Injury. ODC-TBI:769 http://dx.doi.org/10.34945/F5901R
ABSTRACT:
STUDY PURPOSE: Inflammation is a hallmark of traumatic brain injury (TBI) pathophysiology that contributes to both brain damage and its repair. To investigate microglial mechanisms in central and peripheral inflammation following TBI, we inhibited the colony stimulating factor-1 receptor (CSF-1R), critical for microglial survival, with PLX5622 (PLX). We hypothesized that microglia depletion would attenuate central inflammation acutely.
DATA COLLECTED: After randomization, adult male C57BL/6J mice (n = 105) were fed PLX5622 (1200 mg/kg, Plexxikon) or control (AIN-76A rodent chow) diets (21 days) and then received midline fluid percussion injury (mFPI) or sham injury. Blood and brain were collected at 1, 3, or 7 days post-injury (DPI). Immune cell populations (leukocytes, myeloid cells, microglia, monocytes, macrophages, neutrophils) were quantified in the brain and blood by flow cytometry. Pro-inflammatory cytokines (interleukin [IL]-6, IL-1?, tumor necrosis factor [TNF]-?, IFN [interferon]-?) and anti-inflammatory cytokines (IL-10, IL-17A) were quantified in the blood using multiplex ELISA.
CONCLUSIONS: CSF-1R inhibition blunted the immune response to TBI at 1 and 3 day post-injury but elevated peripheral inflammation at 7 days post-injury. CSF-1R inhibition may be a plausible mechanism to target both central and peripheral immune cells and change the long-term inflammatory response to TBI. However, administration of PLX as a research tool to target microglia-mediated inflammation should be used with caution, as we also observed several off-target inflammatory effects of CSF-1R inhibition, independent of brain injury. Specifically, CD115+ peripheral monocytes were depleted.
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DATASET CITATION:
Rowe R. K., Lifshitz J. (2023) Motor, cognitive, anxiety-like, and depressive-like behavior following one or two diffuse TBIs in the mouse. Open Data Commons for Traumatic Brain Injury. ODC-TBI:828 http://dx.doi.org/10.34945/F5BS3R
ABSTRACT:
STUDY PURPOSE: Behavioral impairments can manifest from a single traumatic brain injury (TBI) or repetitive TBI, particularly when subsequent injuries occur before the initial injury heals. We investigated behavior as a primary outcome following TBI.
DATA COLLECTED: Adult (2-4 months old) male C57BL/6 mice received sham or diffuse TBI by midline fluid percussion injury (moderate injury, 1.4 atm). The brain-injured mice received one TBI or two TBIs with an inter-injury interval of approximately 3-9 hours. Motor behavior was tested using the rotarod and modified neurological severity score (NSS) task at 2, 5, and 7 days post-injury. Affective behavioral assessments were tested using novel object recognition (NOR), elevated plus maze, and forced swim task at 7, 14, and/or 28 days post-injury.
CONCLUSIONS: Both a single TBI and repetitive TBI resulted in motor impairments compared to shams as measured by the rotarod and NSS task. Diffuse TBI did not impair cognitive function assessed by NOR. There were also no differences between groups on the elevated plus maze. Repetitive TBI, but not a single TBI, resulted in depressive-like behavior assessed with the forced swim task.
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DATASET CITATION:
Chou A., Lee S., Krukowski K., Guglielmetti C., Nolan A., Hawkins B. E., Chaumeil M. M., Beattie M. S., Bresnahan J. C., Rosi S., Ferguson A. R. (2021) Aggregated animal subject metadata from 11 UCSF preclinical TBI publications and 1 ODC-TBI published dataset. Open Data Commons for Traumatic Brain Injury. ODC-TBI:566 http://dx.doi.org/10.34945/F51P49
ABSTRACT:
STUDY PURPOSE: The dataset was created to provide descriptions of the animal subjects with data uploaded to the ODC-TBI (but not necessarily published yet).
DATA COLLECTED: The metadata was aggregated from 11 papers published from the labs of Susanna Rosi, Michael S Beattie, Jacqueline C Bresnahan, and Adam R Ferguson from UCSF as well as the dataset published by Bridget E Hawkins through the ODC-TBI (DOI:10.34945/F51591). The animal species, strain, sex, genotype and age at time of injury are included in addition to the preclinical TBI model used, the experimental group the subject was assigned to, and the time post-injury of the data entry. The dataset contains a total of N=1250 animals with 3313 observations total. Subject IDs are provided to align this data to the corresponding datasets when they are published.
CONCLUSIONS:
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DATASET CITATION:
Chou A., Krukowski K., Morganti J. M., Riparip L. K., Rosi S. (2022) Peripheral monocyte and resident microglia number and cytokine expression at subchronic timepoints after controlled cortical impact TBI in adult and aged mice. Open Data Commons for Traumatic Brain Injury. ODC-TBI:376 http://dx.doi.org/10.34945/F5T595
ABSTRACT:
STUDY PURPOSE: The purpose of the study was to investigate the effect of age on the inflammatory response of peripheral, infiltrating monocytes after traumatic brain injury.
DATA COLLECTED: The dataset includes several experiments with mice using the parietal controlled cortical impact (CCI) TBI model. A summary of experiments are as follows: (1) Amount of infiltrating monocytes (CD11b+, CD45hi) in the injured brain of wildtype adult (3-4 mo) and aged (18+ mo) mice at 4 and 7 days post-injury (dpi) measured by flow cytommetry. (2) Amount of infiltrating monocyte (CD11b+, CCR2-rfp+) in the injured brain and in the blood of adult and aged (22-24 mo) CCR2-rfp-labeled mice at 4 and 7 dpi measured by flow cytommetry. (3) Amount of newly proliferated infiltrating monocytes (CD11b+, F4/80+, CD45hi) and resident microglia (CD11b+, F4/80+, CD45lo) in the injured brain labeled with BrdU between 3-4 dpi. (4) CCL2, CCL7, CCL8, and CCL12 quantified by qPCR from adult and aged animals at 4 and 7 dpi (normalized to young sham controls). (5) IL-1B, TNFa, iNOS, Ym1, CD206, TGF-B, and IL4Ra inflammatory marker expression measured by qPCR in wildtype adult and aged, Sham and TBI mice at 7 dpi. (6) Radial arm water maze behavior (errors; RAWM) measured at 26-28 dpi in wildtype and CCR2 knockout adult and aged (16-18 mo), Sham and TBI mice. (7) Amount of newly proliferated infiltrating monocytes (CCR2-rfp+) in the blood and bone marrow of adult and aged CCR2-rfp-labeled mice at 4 dpi using EdU labeling and flow cytometry.
CONCLUSIONS:
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DATASET CITATION:
Chou A., Morganti J. M., Jopson T. D., Liu S., Riparip L. K., Guandique C. K., Gupta N., Ferguson A. R., Rosi S. (2022) Cytokine expression and peripheral monocyte infiltration time course and effect of CCR2-antagonist treatment on chronic behavioral outcome in wildtype adult mice after controlled cortical impact TBI. Open Data Commons for Traumatic Brain Injury. ODC-TBI:159 http://dx.doi.org/10.34945/F5PC77
ABSTRACT:
STUDY PURPOSE: The study was designed to study the role of peripheral infiltrating monocytes to traumatic brain injury induced neuroinflammation and outcome.
DATA COLLECTED: The dataset includes several cohorts of wildtype or CX3CR1(gfp/+)/CCR2(rfp/+) transgenic adult (6-7 mo) mice. TBI was induced using the controlled cortical impact model. (1) Transgenic mice were given sham or TBI surgery and samples were collected at 3 hours, 6 hours, 12 hours, 24 hours, 48 hours, 7 days, 14 days, or 28 days post-injury (dpi). Infiltrating monocytes (CD11b+,F4/80+, CCR2-rfp+, CX3CR1-gfp- and CD11b+,F4/80+, CCR2-rfp+, CX3CR1-gfp+) and resident microglia (CD11b+,F4/80+, CCR2-rfp-, CX3CR1-gfp+) numbers were measured by flow cytometry. 14 inflammatory markers were measured from isolated leukocytes in the injured brain via qPCR. (2) Wildtype adult mice were treated with vehicle or a CCR2-antagonist (CCX872). Infiltrating monocytes (CD11b+, CD45hi) were measured by flow cytometry and 18 inflammatory and oxidative stress molecule expression was measured by qPCR at 1 day post-injury (1 dpi). (3) Wildtype mice treated with vehicle or CCR2-antagonist were measured on radial arm water maze (RAWM) performance at 28 dpi.
CONCLUSIONS:
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DATASET CITATION:
Vonder Haar C., Martens K. M., Frankot M. A. (2022) Combined dataset of Rodent Gambling Task in rats after brain injury. Open Data Commons for Traumatic Brain Injury. ODC-TBI:703 http://dx.doi.org/10.34945/F5Q597
ABSTRACT:
STUDY PURPOSE: The goal of this analysis set was to compare data collected across four separate studies, all of which evaluated the effects of traumatic brain injury on the Rodent Gambling Task (RGT). This combined data would have sufficient power to analyze both overall and trial-by-trial outcomes.
DATA COLLECTED: Data were collected across four studies comprising training and testing on the RGT. Three studies were bilateral frontal controlled cortical impact injuries and one was unilateral, parietal controlled cortical impact. Two trained rats before injury, and two after. A total of 109 rats in TBI or Sham conditions (no other manipulations) can be extracted from these data.
Two of these studies are published, one is in review, and one is in preparation for publication.
CONCLUSIONS: Our key finding from the manuscript was that theoretical approaches (sensitivity to overall outcomes vs. sensitivity to immediate outcomes) was less effective at accounting for data than an unbiased k-means clustering approach. The clustering readily identified different phenotypes of decision-making on this task and TBI rats were less likely to be in the "optimal" category and instead were evenly spread across all other categories. The current findings suggest that TBI does not engender a "risky" decision-making trait per se, but rather fundamentally changes the preference for outcomes of rats with injury.
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DATASET CITATION:
Sowers J. L., Sowers M. L., Zhang K., Hawkins B. E. (2021) Traumatic Brain Injury Induces Region-specific Glutamate Metabolism Changes As Measured by Multiple Mass Spectrometry Methods (Animal Metadata). Open Data Commons for Traumatic Brain Injury. ODC-TBI:670 http://dx.doi.org/10.34945/F50P40
ABSTRACT:
STUDY PURPOSE: The purpose of this study was to investigate the early metabolic events occurring in the acute phase of traumatic brain injury (TBI) using multiple mass spectrometry methods
DATA COLLECTED: Data collected was tandem mass tag (TMT) multiplexed based proteomic data acquired from the cortex and hippocampus of injured, sham, and naïve rats. Injured rats were subjected to surgery followed by a fluid percussion injury while sham animals only had surgery. Sham and naïve rats were intubated and mechanically ventilated (isoflurane anesthesia) for similar amounts of time as the FPI injured animals. Adult 3-month-old male Sprague Dawley rats were used for these studies and each animal was housed with one other rat who had similar injury status (sham rats were housed with other sham rats, for example) in a cage with full access to food pellets, water bottle and enrichment material. The brain regions were dissected from the rest of the brain and immediately frozen using dry ice and kept at -80F until processed. The tissues were homogenized separately and labeled with the tandem-mass-tags (TMT) and labeled samples were separated via reverse-phase liquid chromatography and analyzed on a QExactive mass spectrometer. Data was collected at five time points after TBI: 24 hours, 2 weeks, 3 months, 6 months and 1 year. For this study, “Traumatic Brain Injury Induces Region-specific Glutamate Metabolism Changes As Measured by Multiple Mass Spectrometry Methods,” only select proteins from the 24 hour and 2 week time points were used. Whole brain samples for the MALDI-MS imaging study were randomly divided according to injury status and then imaged. See iScience paper for more details on the methods
CONCLUSIONS: We revealed new insights and potential pathways for intervention in acute TBI
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DATASET CITATION:
Sowers J. L., Sowers M. L., Zhang K., Hawkins B. E. (2021) Traumatic Brain Injury Induces Region-specific Glutamate Metabolism Changes As Measured by Multiple Mass Spectrometry Methods. Open Data Commons for Traumatic Brain Injury. ODC-TBI:671 http://dx.doi.org/10.34945/F5W011
ABSTRACT:
STUDY PURPOSE: The purpose of this study was to investigate the early metabolic events occurring in the acute phase of traumatic brain injury (TBI) using multiple mass spectrometry methods
DATA COLLECTED: Data collected was tandem mass tag (TMT) multiplexed based proteomic data acquired from the cortex and hippocampus of injured, sham, and naïve rats. Injured rats were subjected to surgery followed by a fluid percussion injury while sham animals only had surgery. Data was collected at five time points after TBI: 24 hours, 2 weeks, 3 months, 6 months and 1 year. For this study, “Traumatic Brain Injury Induces Region-specific Glutamate Metabolism Changes As Measured by Multiple Mass Spectrometry Methods,” only select proteins from the 24 hour and 2 week time points were used
CONCLUSIONS: We revealed new insights and potential pathways for intervention in acute TBI
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DATASET CITATION:
Morioka K., Marmor Y., Sacramento J. A., Lin A., Shao T., Miclau K. R., Clark D. R., Beattie M. S., Marcucio R. S., Miclau 3rd T., Ferguson A. R., Bresnahan J. C., Bahney C. S. (2021) Humoral and neuronal impacts of traumatic brain injury on fracture healing in mice (polytrauma study). Open Data Commons for Traumatic Brain Injury. ODC-TBI:340 http://dx.doi.org/10.34945/F58596
ABSTRACT:
STUDY PURPOSE: The aim of this polytraumatic study is to evaluate mechanisms that may influence healing in a preclinical murine model of combined fracture and traumatic brain injury (TBI) compared to fracture or TBI alone.
DATA COLLECTED: Experimental Design:
-4 experimental injury conditions (Tibia Fx Only, CCI TBI Only, Ipsilateral Polytrauma, and Contralateral Polytrauma)
-Controlled Cortical Impact parameters: 3.0 mm rounded head, 21 degrees, 2.0mm deep, 150ms dwell time, and 4 m/s velocity
-3 terminal time points (5, 10, and 14 days post-injury)
Outcomes:
1. Quantification of fracture healing: The volume and the composition of the fracture callus, bone, cartilage, vascular tissue, and fibrous tissue were quantified using a microscope and stereology system.
2. Complete blood count: White blood cells, red blood cells, and thrombocytes were counted in cardiac blood.
3. Systemic inflammation: Inflammatory markers (TNF-alpha, IL-1 beta, IL-10, and Arginine) were evaluated by quantitative RT-PCR in spleen tissues.
4. Quantification of lesion area and volume of brain lesion: Gross brain lesion area and brain lesion volume were assessed using a microscope and imaging software.
5. Multivariate analysis of principal component solution: All outcome measures among three fracture groups (Fx Only, Ipsilateral Polytrauma, and Contralateral Polytrauma) at 2-time points ((5 and 10 days post-injury) were integrated into a principal component analysis (PCA). The three first principal components (PC1, PC2, and PC3) were obtained for the interpretation of PC content based on significant PC loading values.
CONCLUSIONS: Our results suggest that a contralateral bone fracture and TBI alter the neuroinflammatory state to accelerate early fracture healing.
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DATASET CITATION:
Andersen, C.R., Wolf, J.T., Jennings, K., Prough, D.S., Hawkins, B.E. (2020) Moody Project Survival Analysis Morris Water Maze Dataset. ODC-TBI:408. DOI:10.34945/F51591
ABSTRACT:
STUDY PURPOSE: To characterize the behavioral consequences of our injury model on Morris Water Maze (MWM) latency with high power from combining animals from 3 studies.
DATA COLLECTED: 46 untreated sham and 61 untreated injured male Sprague-Dawley rats, fluid percussion injury model, learning and memory assessed by spatial hidden platform (3 days of 4 swims per rat per day) Morris water maze; outcome measures analyzed included latency recorded in seconds and number of platforms found.
PRIMARY CONCLUSION: We suggest the Accelerated Failure Time (AFT) models should be the preferred analytical methodology for latency to platform associated with MWM studies.
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