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  1. Article ; Online: Life-long brain compensatory responses to galactic cosmic radiation exposure.

    Miry, Omid / Zhang, Xiao-Lei / Vose, Linnea R / Gopaul, Katisha R / Subah, Galadu / Moncaster, Juliet A / Wojnarowicz, Mark W / Fisher, Andrew M / Tagge, Chad A / Goldstein, Lee E / Stanton, Patric K

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 4292

    Abstract: Galactic cosmic radiation (GCR) composed of high-energy, heavy particles (HZE) poses potentially serious hazards to long-duration crewed missions in deep space beyond earth's magnetosphere, including planned missions to Mars. Chronic effects of GCR ... ...

    Abstract Galactic cosmic radiation (GCR) composed of high-energy, heavy particles (HZE) poses potentially serious hazards to long-duration crewed missions in deep space beyond earth's magnetosphere, including planned missions to Mars. Chronic effects of GCR exposure on brain structure and cognitive function are poorly understood, thereby limiting risk reduction and mitigation strategies to protect against sequelae from exposure during and after deep-space travel. Given the selective vulnerability of the hippocampus to neurotoxic insult and the importance of this brain region to learning and memory, we hypothesized that GCR-relevant HZE exposure may induce long-term alterations in adult hippocampal neurogenesis, synaptic plasticity, and hippocampal-dependent learning and memory. To test this hypothesis, we irradiated 3-month-old male and female mice with a single, whole-body dose of 10, 50, or 100 cGy
    MeSH term(s) Astronauts ; Biomarkers ; Brain/metabolism ; Brain/physiopathology ; Brain/radiation effects ; Cosmic Radiation/adverse effects ; Dentate Gyrus/metabolism ; Dentate Gyrus/physiopathology ; Dentate Gyrus/radiation effects ; Environmental Exposure/adverse effects ; Female ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Hippocampus/radiation effects ; Humans ; Male ; Neurogenesis/radiation effects ; Radiation Exposure/adverse effects ; Space Flight ; Spatial Learning/radiation effects ; Time Factors
    Chemical Substances Biomarkers
    Language English
    Publishing date 2021-02-22
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-83447-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Life-long brain compensatory responses to galactic cosmic radiation exposure

    Omid Miry / Xiao-lei Zhang / Linnea R. Vose / Katisha R. Gopaul / Galadu Subah / Juliet A. Moncaster / Mark W. Wojnarowicz / Andrew M. Fisher / Chad A. Tagge / Lee E. Goldstein / Patric K. Stanton

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 14

    Abstract: Abstract Galactic cosmic radiation (GCR) composed of high-energy, heavy particles (HZE) poses potentially serious hazards to long-duration crewed missions in deep space beyond earth’s magnetosphere, including planned missions to Mars. Chronic effects of ... ...

    Abstract Abstract Galactic cosmic radiation (GCR) composed of high-energy, heavy particles (HZE) poses potentially serious hazards to long-duration crewed missions in deep space beyond earth’s magnetosphere, including planned missions to Mars. Chronic effects of GCR exposure on brain structure and cognitive function are poorly understood, thereby limiting risk reduction and mitigation strategies to protect against sequelae from exposure during and after deep-space travel. Given the selective vulnerability of the hippocampus to neurotoxic insult and the importance of this brain region to learning and memory, we hypothesized that GCR-relevant HZE exposure may induce long-term alterations in adult hippocampal neurogenesis, synaptic plasticity, and hippocampal-dependent learning and memory. To test this hypothesis, we irradiated 3-month-old male and female mice with a single, whole-body dose of 10, 50, or 100 cGy 56Fe ions (600 MeV, 181 keV/μm) at Brookhaven National Laboratory. Our data reveal complex, dynamic, time-dependent effects of HZE exposure on the hippocampus. Two months post exposure, neurogenesis, synaptic plasticity and learning were impaired compared to sham-irradiated, age-matched controls. By six months post-exposure, deficits in spatial learning were absent in irradiated mice, and synaptic potentiation was enhanced. Enhanced performance in spatial learning and facilitation of synaptic plasticity in irradiated mice persisted 12 months post-exposure, concomitant with a dramatic rebound in adult-born neurons. Synaptic plasticity and spatial learning remained enhanced 20 months post-exposure, indicating a life-long influence on plasticity and cognition from a single exposure to HZE in young adulthood. These findings suggest that GCR-exposure can persistently alter brain health and cognitive function during and after long-duration travel in deep space.
    Keywords Medicine ; R ; Science ; Q
    Subject code 150
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Thermal sensitivity of endothelial cells on synthetic vascular graft material.

    Brinton, Mark R / Tagge, Chad A / Stewart, Russell J / Cheung, Alfred K / Shiu, Yan-Ting E / Christensen, Douglas A

    International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group

    2012  Volume 28, Issue 2, Page(s) 163–174

    Abstract: Purpose: The goal is to identify thermal exposures capable of reducing or eliminating cell survival on expanded polytetrafluoroethylene (ePTFE), in an effort to develop a mild hyperthermia treatment of neointimal hyperplasia in ePTFE vascular grafts.: ...

    Abstract Purpose: The goal is to identify thermal exposures capable of reducing or eliminating cell survival on expanded polytetrafluoroethylene (ePTFE), in an effort to develop a mild hyperthermia treatment of neointimal hyperplasia in ePTFE vascular grafts.
    Materials and methods: Viable and dead bovine aortic endothelial cells were quantified following different thermal exposure conditions: cells on collagen-coated ePTFE sheets or tissue culture polystyrene dishes were heated at 42° and 45°C to determine their thermal sensitivity on different surfaces, and cells cultured on collagen-coated ePTFE sheets were heated at 43-50°C for various durations, followed by incubation at 37°C for 0 and 20 h, respectively. Significant cell death was set to be 50%. Two types of cell death, apoptosis and necrosis, were distinguished by cell morphology and membrane integrity assessments.
    Results: The attachment and survival of cells on ePTFE sheets were more sensitive to inhibition by mild heating than those on tissue culture dishes. Exposure to 45°C for 90 min and 50°C for 30 min caused significant necrotic cell death on ePTFE (65% and 75%, respectively). A 37°C/20-h incubation following 30-min exposures at 47° and 50°C increased total cell death (necrosis + apoptosis) from 20% to 50% and 75% to 100%, respectively.
    Conclusion: Cells grown on ePTFE were more susceptible to mild hyperthermia-induced death, compared to those on tissue culture dishes. Significant cell death on ePTFE mainly via apoptosis can be achieved by optimising temperature and duration of exposure.
    MeSH term(s) Animals ; Blood Vessel Prosthesis ; Cattle ; Cell Death ; Cells, Cultured ; Coated Materials, Biocompatible ; Endothelial Cells ; Endothelium, Vascular/cytology ; Hot Temperature ; Hyperplasia/pathology ; Hyperplasia/prevention & control ; Polytetrafluoroethylene ; Tunica Intima/pathology ; Vascular Grafting/methods
    Chemical Substances Coated Materials, Biocompatible ; Polytetrafluoroethylene (9002-84-0)
    Language English
    Publishing date 2012-01-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 632526-9
    ISSN 1464-5157 ; 0265-6736
    ISSN (online) 1464-5157
    ISSN 0265-6736
    DOI 10.3109/02656736.2011.638963
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model.

    Tagge, Chad A / Fisher, Andrew M / Minaeva, Olga V / Gaudreau-Balderrama, Amanda / Moncaster, Juliet A / Zhang, Xiao-Lei / Wojnarowicz, Mark W / Casey, Noel / Lu, Haiyan / Kokiko-Cochran, Olga N / Saman, Sudad / Ericsson, Maria / Onos, Kristen D / Veksler, Ronel / Senatorov, Vladimir V / Kondo, Asami / Zhou, Xiao Z / Miry, Omid / Vose, Linnea R /
    Gopaul, Katisha R / Upreti, Chirag / Nowinski, Christopher J / Cantu, Robert C / Alvarez, Victor E / Hildebrandt, Audrey M / Franz, Erich S / Konrad, Janusz / Hamilton, James A / Hua, Ning / Tripodis, Yorghos / Anderson, Andrew T / Howell, Gareth R / Kaufer, Daniela / Hall, Garth F / Lu, Kun P / Ransohoff, Richard M / Cleveland, Robin O / Kowall, Neil W / Stein, Thor D / Lamb, Bruce T / Huber, Bertrand R / Moss, William C / Friedman, Alon / Stanton, Patric K / McKee, Ann C / Goldstein, Lee E

    Brain : a journal of neurology

    2018  Volume 141, Issue 2, Page(s) 422–458

    Abstract: The mechanisms underpinning concussion, traumatic brain injury, and chronic traumatic encephalopathy, and the relationships between these disorders, are poorly understood. We examined post-mortem brains from teenage athletes in the acute-subacute period ... ...

    Abstract The mechanisms underpinning concussion, traumatic brain injury, and chronic traumatic encephalopathy, and the relationships between these disorders, are poorly understood. We examined post-mortem brains from teenage athletes in the acute-subacute period after mild closed-head impact injury and found astrocytosis, myelinated axonopathy, microvascular injury, perivascular neuroinflammation, and phosphorylated tau protein pathology. To investigate causal mechanisms, we developed a mouse model of lateral closed-head impact injury that uses momentum transfer to induce traumatic head acceleration. Unanaesthetized mice subjected to unilateral impact exhibited abrupt onset, transient course, and rapid resolution of a concussion-like syndrome characterized by altered arousal, contralateral hemiparesis, truncal ataxia, locomotor and balance impairments, and neurobehavioural deficits. Experimental impact injury was associated with axonopathy, blood-brain barrier disruption, astrocytosis, microgliosis (with activation of triggering receptor expressed on myeloid cells, TREM2), monocyte infiltration, and phosphorylated tauopathy in cerebral cortex ipsilateral and subjacent to impact. Phosphorylated tauopathy was detected in ipsilateral axons by 24 h, bilateral axons and soma by 2 weeks, and distant cortex bilaterally at 5.5 months post-injury. Impact pathologies co-localized with serum albumin extravasation in the brain that was diagnostically detectable in living mice by dynamic contrast-enhanced MRI. These pathologies were also accompanied by early, persistent, and bilateral impairment in axonal conduction velocity in the hippocampus and defective long-term potentiation of synaptic neurotransmission in the medial prefrontal cortex, brain regions distant from acute brain injury. Surprisingly, acute neurobehavioural deficits at the time of injury did not correlate with blood-brain barrier disruption, microgliosis, neuroinflammation, phosphorylated tauopathy, or electrophysiological dysfunction. Furthermore, concussion-like deficits were observed after impact injury, but not after blast exposure under experimental conditions matched for head kinematics. Computational modelling showed that impact injury generated focal point loading on the head and seven-fold greater peak shear stress in the brain compared to blast exposure. Moreover, intracerebral shear stress peaked before onset of gross head motion. By comparison, blast induced distributed force loading on the head and diffuse, lower magnitude shear stress in the brain. We conclude that force loading mechanics at the time of injury shape acute neurobehavioural responses, structural brain damage, and neuropathological sequelae triggered by neurotrauma. These results indicate that closed-head impact injuries, independent of concussive signs, can induce traumatic brain injury as well as early pathologies and functional sequelae associated with chronic traumatic encephalopathy. These results also shed light on the origins of concussion and relationship to traumatic brain injury and its aftermath.awx350media15713427811001.
    MeSH term(s) Action Potentials/physiology ; Adolescent ; Animals ; Athletes ; Athletic Injuries/complications ; Brain/pathology ; Brain Concussion/etiology ; Calcium-Binding Proteins ; Cohort Studies ; Computer Simulation ; Craniocerebral Trauma/complications ; Craniocerebral Trauma/diagnostic imaging ; Craniocerebral Trauma/etiology ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Female ; Gene Expression Regulation/physiology ; Hippocampus/physiopathology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins ; Models, Neurological ; Prefrontal Cortex/physiopathology ; Receptors, CCR2/genetics ; Receptors, CCR2/metabolism ; Receptors, Interleukin-8A/genetics ; Receptors, Interleukin-8A/metabolism ; Tauopathies/etiology ; Vascular System Injuries/etiology ; Young Adult
    Chemical Substances AIF1 protein, human ; Calcium-Binding Proteins ; Ccr2 protein, mouse ; DNA-Binding Proteins ; Microfilament Proteins ; Receptors, CCR2 ; Receptors, Interleukin-8A
    Language English
    Publishing date 2018-01-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awx350
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui II Zs.26: Show issues Location:
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  5. Article ; Online: Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model.

    Goldstein, Lee E / Fisher, Andrew M / Tagge, Chad A / Zhang, Xiao-Lei / Velisek, Libor / Sullivan, John A / Upreti, Chirag / Kracht, Jonathan M / Ericsson, Maria / Wojnarowicz, Mark W / Goletiani, Cezar J / Maglakelidze, Giorgi M / Casey, Noel / Moncaster, Juliet A / Minaeva, Olga / Moir, Robert D / Nowinski, Christopher J / Stern, Robert A / Cantu, Robert C /
    Geiling, James / Blusztajn, Jan K / Wolozin, Benjamin L / Ikezu, Tsuneya / Stein, Thor D / Budson, Andrew E / Kowall, Neil W / Chargin, David / Sharon, Andre / Saman, Sudad / Hall, Garth F / Moss, William C / Cleveland, Robin O / Tanzi, Rudolph E / Stanton, Patric K / McKee, Ann C

    Science translational medicine

    2012  Volume 4, Issue 134, Page(s) 134ra60

    Abstract: Blast exposure is associated with traumatic brain injury (TBI), neuropsychiatric symptoms, and long-term cognitive disability. We examined a case series of postmortem brains from U.S. military veterans exposed to blast and/or concussive injury. We found ... ...

    Abstract Blast exposure is associated with traumatic brain injury (TBI), neuropsychiatric symptoms, and long-term cognitive disability. We examined a case series of postmortem brains from U.S. military veterans exposed to blast and/or concussive injury. We found evidence of chronic traumatic encephalopathy (CTE), a tau protein-linked neurodegenerative disease, that was similar to the CTE neuropathology observed in young amateur American football players and a professional wrestler with histories of concussive injuries. We developed a blast neurotrauma mouse model that recapitulated CTE-linked neuropathology in wild-type C57BL/6 mice 2 weeks after exposure to a single blast. Blast-exposed mice demonstrated phosphorylated tauopathy, myelinated axonopathy, microvasculopathy, chronic neuroinflammation, and neurodegeneration in the absence of macroscopic tissue damage or hemorrhage. Blast exposure induced persistent hippocampal-dependent learning and memory deficits that persisted for at least 1 month and correlated with impaired axonal conduction and defective activity-dependent long-term potentiation of synaptic transmission. Intracerebral pressure recordings demonstrated that shock waves traversed the mouse brain with minimal change and without thoracic contributions. Kinematic analysis revealed blast-induced head oscillation at accelerations sufficient to cause brain injury. Head immobilization during blast exposure prevented blast-induced learning and memory deficits. The contribution of blast wind to injurious head acceleration may be a primary injury mechanism leading to blast-related TBI and CTE. These results identify common pathogenic determinants leading to CTE in blast-exposed military veterans and head-injured athletes and additionally provide mechanistic evidence linking blast exposure to persistent impairments in neurophysiological function, learning, and memory.
    MeSH term(s) Acceleration ; Adolescent ; Adult ; Animals ; Athletes ; Axons/pathology ; Behavior, Animal ; Blast Injuries/complications ; Blast Injuries/pathology ; Blast Injuries/physiopathology ; Brain Concussion/complications ; Brain Concussion/pathology ; Brain Concussion/physiopathology ; Brain Injury, Chronic/complications ; Brain Injury, Chronic/pathology ; Brain Injury, Chronic/physiopathology ; Disease Models, Animal ; Head/pathology ; Head/physiopathology ; Hippocampus/pathology ; Hippocampus/physiopathology ; Hippocampus/ultrastructure ; Humans ; Intracranial Pressure ; Long-Term Potentiation ; Male ; Mice ; Middle Aged ; Military Personnel/psychology ; Phosphorylation ; Postmortem Changes ; Synaptic Transmission ; Veterans/psychology ; Young Adult ; tau Proteins/metabolism
    Chemical Substances tau Proteins
    Language English
    Publishing date 2012-05-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.3003716
    Database MEDical Literature Analysis and Retrieval System OnLINE

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