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  1. Article ; Online: General Anesthesia Blocks Pain-Induced Hemorrhage and Locomotor Deficits After Spinal Cord Injury in Rats.

    Davis, Jacob A / Bopp, Anne C / Henwood, Melissa K / Bean, Paris / Grau, James W

    Journal of neurotrauma

    2023  Volume 40, Issue 23-24, Page(s) 2552–2565

    Abstract: Research has shown that engaging pain (nociceptive) pathways after spinal cord injury (SCI) aggravates secondary injury and undermines locomotor recovery. This is significant because SCI is commonly accompanied by additional tissue damage (polytrauma) ... ...

    Abstract Research has shown that engaging pain (nociceptive) pathways after spinal cord injury (SCI) aggravates secondary injury and undermines locomotor recovery. This is significant because SCI is commonly accompanied by additional tissue damage (polytrauma) that drives nociceptive activity. Cutting communication with the brain by means of a surgical transection, or pharmacologically transecting the cord by slowly infusing a sodium channel blocker (lidocaine) rostral to a thoracic contusion, blocks pain-induced hemorrhage. These observations suggest that the adverse effect of pain after SCI depends on supraspinal (brain) systems. We hypothesize that inhibiting brain activity using a general anesthetic (e.g., pentobarbital, isoflurane) should have a protective effect. The present study shows that placing rats in an anesthetic state with pentobarbital or isoflurane 24 h after a lower thoracic contusion injury blocks pain-induced intraspinal inflammation and hemorrhage when administered before pain. Pentobarbital also extends protective effects against locomotor deficits produced by noxious stimulation. Inducing anesthesia after noxious stimulation, however, has no effect. Similarly, subanesthetic dosages of pentobarbital were also ineffective at blocking pain-induced hemorrhage. Also examined were the hemodynamic impacts of both pain and anesthetic delivery after SCI. Peripheral pain-input induced an acute increase in systolic blood pressure; isoflurane and pentobarbital prevent this increase, which may contribute to the protective effect of anesthesia. The results suggest that placing patients with SCI in a state akin to a medically induced coma can have a protective effect that blocks the adverse effects of pain.
    MeSH term(s) Humans ; Rats ; Animals ; Pentobarbital ; Isoflurane/pharmacology ; Pain/drug therapy ; Pain/etiology ; Spinal Cord Injuries/complications ; Anesthetics ; Anesthesia, General/adverse effects ; Hemorrhage ; Contusions/complications
    Chemical Substances Pentobarbital (I4744080IR) ; Isoflurane (CYS9AKD70P) ; Anesthetics
    Language English
    Publishing date 2023-04-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 645092-1
    ISSN 1557-9042 ; 0897-7151
    ISSN (online) 1557-9042
    ISSN 0897-7151
    DOI 10.1089/neu.2022.0449
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Strength of spatial correlation between gray matter connectivity and patterns of proto-oncogene and neural network construction gene expression is associated with diffuse glioma survival.

    Kesler, Shelli R / Harrison, Rebecca A / Schutz, Alexa De La Torre / Michener, Hayley / Bean, Paris / Vallone, Veronica / Prinsloo, Sarah

    Frontiers in neurology

    2024  Volume 15, Page(s) 1345520

    Abstract: Introduction: Like other forms of neuropathology, gliomas appear to spread along neural pathways. Accordingly, our group and others have previously shown that brain network connectivity is highly predictive of glioma survival. In this study, we aimed to ...

    Abstract Introduction: Like other forms of neuropathology, gliomas appear to spread along neural pathways. Accordingly, our group and others have previously shown that brain network connectivity is highly predictive of glioma survival. In this study, we aimed to examine the molecular mechanisms of this relationship via imaging transcriptomics.
    Methods: We retrospectively obtained presurgical, T1-weighted MRI datasets from 669 adult patients, newly diagnosed with diffuse glioma. We measured brain connectivity using gray matter networks and coregistered these data with a transcriptomic brain atlas to determine the spatial co-localization between brain connectivity and expression patterns for 14 proto-oncogenes and 3 neural network construction genes.
    Results: We found that all 17 genes were significantly co-localized with brain connectivity (
    Discussion: Our findings provide novel insights regarding how gene-brain connectivity interactions may affect glioma survival.
    Language English
    Publishing date 2024-03-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2024.1345520
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Strength of spatial correlation between structural brain network connectivity and brain-wide patterns of proto-oncogene and neural network construction gene expression is associated with diffuse glioma survival.

    Kesler, Shelli R / Harrison, Rebecca A / Schultz, Alexa De La Torre / Michener, Hayley / Bean, Paris / Vallone, Veronica / Prinsloo, Sarah

    medRxiv : the preprint server for health sciences

    2023  

    Abstract: Like other forms of neuropathology, gliomas appear to spread along neural pathways. Accordingly, our group and others have previously shown that brain network connectivity is highly predictive of glioma survival. In this study, we aimed to examine the ... ...

    Abstract Like other forms of neuropathology, gliomas appear to spread along neural pathways. Accordingly, our group and others have previously shown that brain network connectivity is highly predictive of glioma survival. In this study, we aimed to examine the molecular mechanisms of this relationship via imaging transcriptomics. We retrospectively obtained presurgical, T1-weighted MRI datasets from 669 adult patients, newly diagnosed with diffuse glioma. We measured brain connectivity using gray matter networks and coregistered these data with a transcriptomic brain atlas to determine the spatial co-localization between brain connectivity and expression patterns for 14 proto-oncogenes and 3 neural network construction genes. We found that all 17 genes were significantly co-localized with brain connectivity (p < 0.03, corrected). The strength of co-localization was highly predictive of overall survival in a cross-validated Cox Proportional Hazards model (mean area under the curve, AUC = 0.68 +/- 0.01) and significantly (p < 0.001) more so for a random forest survival model (mean AUC = 0.97 +/- 0.06). Bayesian network analysis demonstrated direct and indirect causal relationships among gene-brain co-localizations and survival. Gene ontology analysis showed that metabolic processes were overexpressed when spatial co-localization between brain connectivity and gene transcription was highest (p < 0.001). Drug-gene interaction analysis identified 84 potential candidate therapies based on our findings. Our findings provide novel insights regarding how gene-brain connectivity interactions may affect glioma survival.
    Language English
    Publishing date 2023-11-28
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.11.27.23299085
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Learning to promote recovery after spinal cord injury.

    Grau, James W / Baine, Rachel E / Bean, Paris A / Davis, Jacob A / Fauss, Gizelle N / Henwood, Melissa K / Hudson, Kelsey E / Johnston, David T / Tarbet, Megan M / Strain, Misty M

    Experimental neurology

    2020  Volume 330, Page(s) 113334

    Abstract: The present review explores the concept of learning within the context of neurorehabilitation after spinal cord injury (SCI). The aim of physical therapy and neurorehabilitation is to bring about a lasting change in function-to encourage learning. ... ...

    Abstract The present review explores the concept of learning within the context of neurorehabilitation after spinal cord injury (SCI). The aim of physical therapy and neurorehabilitation is to bring about a lasting change in function-to encourage learning. Traditionally, it was assumed that the adult spinal cord is hardwired-immutable and incapable of learning. Research has shown that neurons within the lower (lumbosacral) spinal cord can support learning after communication with the brain has been disrupted by means of a thoracic transection. Noxious stimulation can sensitize nociceptive circuits within the spinal cord, engaging signal pathways analogous to those implicated in brain-dependent learning and memory. After a spinal contusion injury, pain input can fuel hemorrhage, increase the area of tissue loss (secondary injury), and undermine long-term recovery. Neurons within the spinal cord are sensitive to environmental relations. This learning has a metaplastic effect that counters neural over-excitation and promotes adaptive learning through an up-regulation of brain-derived neurotrophic factor (BDNF). Exposure to rhythmic stimulation, treadmill training, and cycling also enhances the expression of BDNF and counters the development of nociceptive sensitization. SCI appears to enable plastic potential within the spinal cord by down-regulating the Cl
    MeSH term(s) Animals ; Humans ; Learning/physiology ; Neuronal Plasticity/physiology ; Recovery of Function/physiology ; Spinal Cord Injuries/physiopathology ; Spinal Cord Injuries/rehabilitation
    Language English
    Publishing date 2020-04-28
    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. ; Review
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2020.113334
    Database MEDical Literature Analysis and Retrieval System OnLINE

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