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  1. Article ; Online: Introducing

    Bramlett, Helen M

    Neurotrauma reports

    2020  Volume 1, Issue 1, Page(s) 1

    Language English
    Publishing date 2020-07-23
    Document type Editorial
    ISSN 2689-288X
    ISSN (online) 2689-288X
    DOI 10.1089/neur.2020.28999.hb.editorial
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  2. Article ; Online: COVID-19 Deterred Career Path of Our Undergraduate Neuroscience Students: Educators' Perspective.

    Raval, Ami P / Bramlett, Helen M

    eNeuro

    2022  Volume 9, Issue 5

    MeSH term(s) COVID-19 ; Humans ; Students
    Language English
    Publishing date 2022-10-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0384-22.2022
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  3. Article ; Online: Introduction to the special issue on neurological disorders across the female life span.

    Raval, Ami P / Bramlett, Helen M

    Neurobiology of disease

    2022  Volume 174, Page(s) 105886

    MeSH term(s) Female ; Humans ; Longevity ; Nervous System Diseases/therapy
    Language English
    Publishing date 2022-10-07
    Publishing country United States
    Document type Editorial ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2022.105886
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4444: Show issues Location:
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  4. Article ; Online: Increasing Rigor of Preclinical Research to Maximize Opportunities for Translation.

    Radabaugh, Hannah L / Ferguson, Adam R / Bramlett, Helen M / Dietrich, W Dalton

    Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

    2023  Volume 20, Issue 6, Page(s) 1433–1445

    Abstract: The use of animal models in pre-clinical research has significantly broadened our understanding of the pathologies that underlie traumatic brain injury (TBI)-induced damage and deficits. However, despite numerous pre-clinical studies reporting the ... ...

    Abstract The use of animal models in pre-clinical research has significantly broadened our understanding of the pathologies that underlie traumatic brain injury (TBI)-induced damage and deficits. However, despite numerous pre-clinical studies reporting the identification of promising neurotherapeutics, translation of these therapies to clinical application has so far eluded the TBI research field. A concerted effort to address this lack of translatability is long overdue. Given the inherent heterogeneity of TBI and the replication crisis that continues to plague biomedical research, this is a complex task that will require a multifaceted approach centered around rigor and reproducibility. Here, we discuss the role of three primary focus areas for better aligning pre-clinical research with clinical TBI management. These focus areas are (1) reporting and standardization of protocols, (2) replication of prior knowledge including the confirmation of expected pharmacodynamics, and (3) the broad application of open science through inter-center collaboration and data sharing. We further discuss current efforts that are establishing the core framework needed for successfully addressing the translatability crisis of TBI.
    MeSH term(s) Animals ; Reproducibility of Results ; Brain Injuries, Traumatic/therapy ; Brain Injuries, Traumatic/pathology ; Brain Injuries/pathology ; Biomedical Research
    Language English
    Publishing date 2023-07-31
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2316693-9
    ISSN 1878-7479 ; 1933-7213
    ISSN (online) 1878-7479
    ISSN 1933-7213
    DOI 10.1007/s13311-023-01400-5
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  5. Article ; Online: Traumatic brain injury in women across lifespan.

    Blaya, Meghan O / Raval, Ami P / Bramlett, Helen M

    Neurobiology of disease

    2022  Volume 164, Page(s) 105613

    Abstract: Traumatic brain injury (TBI) is a leading cause of death and disability and a global public health challenge. Every year more than 50 million people suffer a TBI, and it is estimated that 50% of the global population will experience at least one TBI in ... ...

    Abstract Traumatic brain injury (TBI) is a leading cause of death and disability and a global public health challenge. Every year more than 50 million people suffer a TBI, and it is estimated that 50% of the global population will experience at least one TBI in their lifetime. TBI affects both men and women of all ages, however there is a male bias in TBI research as women have frequently been left out of the literature despite irrefutable evidence of male and female dimorphism in several posttraumatic measures. Women uniquely experience distinct life stages marked by levels of endogenous circulating sex hormones, as well as by physiological changes that are nonexistent in men. In addition to generalized sex-specific differences, a woman's susceptibility, neurological outcomes, and treatment success may vary considerably depending upon when in her lifespan she incurred a traumatic insult. How women impacted by TBI might differ from other women as a factor of age and physiology is not well understood. Furthermore, there is a gap in the knowledge of what happens when TBI occurs in the presence of certain sex-specific and sex-nonspecific variables, such as during pregnancy, with oral contraceptive use, in athletics, in cases of addiction and nicotine consumption, during perimenopause, postmenopause, in frailty, among others. Parsing out how hormone-dependent and hormone-independent lifespan variables may influence physiological, neurodegenerative, and functional outcomes will greatly contribute to future investigative studies and direct therapeutic strategies. The goal of this review is to aggregate the knowledge of prevalence, prognosis, comorbid risk, and response of women incurring TBI at differing phases of lifespan. We strive to illuminate commonalities and disparities among female populations, and to pose important questions to highlight gaps in the field in order to further the endeavor of targeted treatment interventions in a patient-specific manner.
    MeSH term(s) Age Factors ; Brain Injuries, Traumatic/epidemiology ; Female ; Humans ; Longevity ; Pregnancy ; Prognosis
    Language English
    Publishing date 2022-01-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2022.105613
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4444: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Electronic Cigarette Vape Exposure Exacerbates Post-Ischemic Outcomes in Female but Not in Male Rats.

    Pradhyumnan, Hari / Patel, Shahil H / Furones-Alonso, Ofelia / Zhao, Weizhao / Bramlett, Helen M / Raval, Ami P

    Stroke

    2024  Volume 55, Issue 3, Page(s) 735–746

    Abstract: Background: Nicotine-containing electronic cigarette (EC) vaping has become popular worldwide, and our understanding of the effects of vaping on stroke outcomes is elusive. Using a rat model of transient middle cerebral artery occlusion, the current ... ...

    Abstract Background: Nicotine-containing electronic cigarette (EC) vaping has become popular worldwide, and our understanding of the effects of vaping on stroke outcomes is elusive. Using a rat model of transient middle cerebral artery occlusion, the current exploratory study aims to evaluate the sex-dependent effects of EC exposure on brain energy metabolism and stroke outcomes.
    Methods: Adult Sprague-Dawley rats of both sexes were randomly assigned to air/EC vapor (5% nicotine Juul pods) exposure for 16 nights, followed by randomization into 3 cohorts. The first cohort underwent exposure to air/EC preceding randomization to transient middle cerebral artery occlusion (90 minutes) or sham surgery, followed by survival for 21 days. During the survival period, rats underwent sensorimotor and Morris water maze testing. Subsequently, brains were collected for histopathology. A second cohort was exposed to air/EC after which brains were collected for unbiased metabolomics analysis. The third cohort of animals was exposed to air/EC and received transient middle cerebral artery occlusion/sham surgery, and brain tissue was collected 24 hours later for biochemical analysis.
    Results: In females, EC significantly increased (
    Conclusions: Even brief EC exposure over 2 weeks impacts brain energy metabolism, exacerbates infarction, and worsens poststroke cognitive deficits in working memory more in female than male rats.
    MeSH term(s) Humans ; Adult ; Rats ; Male ; Female ; Animals ; Vaping ; Rats, Sprague-Dawley ; Nicotine/adverse effects ; Electronic Nicotine Delivery Systems ; Infarction, Middle Cerebral Artery/metabolism
    Chemical Substances Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80381-9
    ISSN 1524-4628 ; 0039-2499 ; 0749-7954
    ISSN (online) 1524-4628
    ISSN 0039-2499 ; 0749-7954
    DOI 10.1161/STROKEAHA.123.046101
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    Zs.A 448: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  7. Article ; Online: Beneficial Effects of Human Schwann Cell-Derived Exosomes in Mitigating Secondary Damage After Penetrating Ballistic-Like Brain Injury.

    Nishimura, Kengo / Sanchez-Molano, Juliana / Kerr, Nadine / Pressman, Yelena / Silvera, Risset / Khan, Aisha / Gajavelli, Shyam / Bramlett, Helen M / Dietrich, W Dalton

    Journal of neurotrauma

    2024  

    Abstract: There is a growing body of evidence that the delivery of cell-derived exosomes normally involved in intracellular communication can reduce secondary injury mechanisms after brain and spinal cord injury and improve outcomes. Exosomes are nanometer-sized ... ...

    Abstract There is a growing body of evidence that the delivery of cell-derived exosomes normally involved in intracellular communication can reduce secondary injury mechanisms after brain and spinal cord injury and improve outcomes. Exosomes are nanometer-sized vesicles that are released by Schwann cells and may have neuroprotective effects by reducing post-traumatic inflammatory processes as well as promoting tissue healing and functional recovery. The purpose of this study was to evaluate the beneficial effects of human Schwann-cell exosomes (hSC-Exos) in a severe model of penetrating ballistic-like brain injury (PBBI) in rats and investigate effects on multiple outcomes. Human Schwann cell processing protocols followed Current Good Manufacturing Practices (cGMP) with exosome extraction and purification steps approved by the Food and Drug Administration for an expanded access single ALS patient Investigational New Drug. Anesthetized male Sprague-Dawley rats (280-350g) underwent PBBI surgery or Sham procedures and, starting 30 min after injury, received either a dose of hSC-Exos or phosphate-buffered saline through the jugular vein. At 48h after PBBI, flow cytometry analysis of cortical tissue revealed that hSC-Exos administration reduced the number of activated microglia and levels of caspase-1, a marker of inflammasome activation. Neuropathological analysis at 21 days showed that hSC-Exos treatment after PBBI significantly reduced overall contusion volume and decreased the frequency of Iba-1 positive activated and amoeboid microglia by immunocytochemical analysis. This study revealed that the systemic administration of hSC-Exos is neuroprotective in a model of severe TBI and reduces secondary inflammatory injury mechanisms and histopathological damage. The administration of hSC-Exos represents a clinically relevant cell-based therapy to limit the detrimental effects of neurotrauma or other progressive neurological injuries by impacting multiple pathophysiological events and promoting neurological recovery.
    Language English
    Publishing date 2024-04-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645092-1
    ISSN 1557-9042 ; 0897-7151
    ISSN (online) 1557-9042
    ISSN 0897-7151
    DOI 10.1089/neu.2023.0650
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    Zs.A 2016: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  8. Article ; Online: Dose-dependent modulation of microglia activation in rats after penetrating traumatic brain injury (pTBI) by transplanted human neural stem cells.

    Andreu, MaryLourdes / Matti, Nathalie / Bramlett, Helen M / Shi, Yan / Gajavelli, Shyam / Dietrich, W Dalton

    PloS one

    2023  Volume 18, Issue 5, Page(s) e0285633

    Abstract: Traumatic brain injury (TBI) often results in long-lasting patterns of neurological deficits including motor, sensory, and cognitive abnormalities. Cranial gunshot survivors are among the most disabled TBI patients and face a lifetime of disability with ... ...

    Abstract Traumatic brain injury (TBI) often results in long-lasting patterns of neurological deficits including motor, sensory, and cognitive abnormalities. Cranial gunshot survivors are among the most disabled TBI patients and face a lifetime of disability with no approved strategies to protect or repair the brain after injury. Recent studies using a model of penetrating TBI (pTBI) have reported that human neural stem cells (hNSCs) transplantation can lead to dose and location-dependent neuroprotection. Evidence for regional patterns of microglial activation has also been reported after pTBI with evidence for microglial cell death by pyroptosis. Because of the importance of injury-induced microglial activation in the pathogenesis of TBI, we tested the hypothesis that dose-dependent hNSC mediated neuroprotection after pTBI was associated with reduced microglial activation in pericontusional cortical areas. To test this hypothesis, quantitative microglial/macrophage Iba1 immunohistochemistry and Sholl analysis was conducted to investigate the arborization patterns using four experimental groups including, (i) Sham operated (no injury) + low dose (0.16 million cells/rat), (ii) pTBI + vehicle (no cells), (iii) pTBI + low dose hNSCs (0.16 million/rat), and (iv) pTBI + high dose hNSCs (1.6 million cells/rat). At 3 months post-transplantation (transplants at one week after pTBI), the total number of intersections was significantly reduced in vehicle treated pTBI animals versus sham operated controls indicating increased microglia/macrophage activation. In contrast, hNSC transplantation led to a dose-dependent increase in the number of intersections compared to pTBI vehicle indicating less microglia/macrophage activation. The peak of Sholl intersections at 1 μm from the center of the microglia/macrophages ranged from ~6,500-14,000 intersections for sham operated, ~250-500 intersections for pTBI vehicle, ~550-1,000 intersections for pTBI low dose, and ~2,500-7,500 intersections for pTBI high dose. Plotting data along the rostrocaudal axis also showed that pericontusional cortical areas protected by hNSC transplantation had increased intersections compared to nontreated pTBI animals. These studies using a non-biased Sholl analysis demonstrated a dose-dependent reduction in inflammatory cell activation that may be associated with a neuroprotective effect driven by the cellular transplant in perilesional regions after pTBI.
    MeSH term(s) Humans ; Rats ; Animals ; Microglia/metabolism ; Macrophage Activation ; Brain Injuries, Traumatic/pathology ; Neural Stem Cells/metabolism ; Brain/metabolism ; Disease Models, Animal
    Language English
    Publishing date 2023-05-16
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0285633
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  9. Article ; Online: Determinants of pneumonia during endovascular hypothermia: editorial commentary on Lyden et al., 2013.

    Bramlett, Helen M

    Therapeutic hypothermia and temperature management

    2013  Volume 3, Issue 2, Page(s) 52–53

    Language English
    Publishing date 2013-05-28
    Publishing country United States
    Document type Editorial
    ZDB-ID 2609342-X
    ISSN 2153-7933 ; 2153-7658
    ISSN (online) 2153-7933
    ISSN 2153-7658
    DOI 10.1089/ther.2013.0011
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  10. Article ; Online: Special issue of translational stroke: importance of sex in the pathophysiology and treatment of acute CNS repair.

    Bramlett, Helen M

    Translational stroke research

    2013  Volume 4, Issue 4, Page(s) 379–380

    MeSH term(s) Animals ; Central Nervous System Diseases/etiology ; Central Nervous System Diseases/therapy ; Female ; Humans ; Male ; Sex Factors ; Stroke/etiology ; Stroke/therapy
    Language English
    Publishing date 2013-05-25
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2541897-X
    ISSN 1868-601X ; 1868-4483
    ISSN (online) 1868-601X
    ISSN 1868-4483
    DOI 10.1007/s12975-013-0264-3
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