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Traumatic Brain Injury - Europe PMC

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Last Updated: 18 May 2022

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A three-dimensional matrix system containing melatonin and neural stem cells repairs damage from traumatic brain injury in rats.

Brain lesions can cause neural stem cells to emerge, proliferate, distinguish, and migrate to the injured area. However, after severe brain injury, brain tissue loss, and microenvironment changes, neural stem cell survival and development are greatly harmed; the resulting decrease in the number of neural stem cells hinders proper repair of the injured area. We therefore investigated the therapeutic effects of melatonin and neural stem cells on traumatic brain injury in rats. Compared to Matrigel alone, neural stem cells alone, Matrigel and neural stem cells combined, and Matrigel and melatonin together, we found that treatment with melatonin and neural stem cells reduced brain lesion volume, increased the number of living neurons, and enhanced neurological function, as well as improved neurological function.

Source link: https://europepmc.org/article/MED/35535904


The endogenous progenitor response following traumatic brain injury: a target for cell therapy paradigms.

Although there is ample evidence that central nervous system progenitor pools respond to traumatic brain injury, the reported results are variable and may influence both recovery and pathophysiology. Both the hippocampal dentate gyrus and subventricular zone of the lateral ventricles, as well as circumventricular organs, are also discussed as endogenous repair targets. The stimulation of endogenous neurogenesis remains a promising treatment for recovery after traumatic brain injury, with increased knowledge and a more targeted strategy.

Source link: https://europepmc.org/article/MED/35535870


Status of precision medicine approaches to traumatic brain injury.

Traumatic brain injury is a serious condition in which head trauma causes brain damage, resulting in a loss of brain function, which results in a disruption of brain function. TBIs can range in severity from mild to severe, and can be complicated by the fact that some people have multiple TBIs, which is a risk factor for poor long-term outcomes. In one person, a blow of similar strength will have only mild, primary outcomes, but it can have severe, chronic consequences in another. Many researchers have started to investigate the possibility of using precision medicine techniques to address TBI therapy, which has resulted in a variety of studies. We'll explore in this article how to determine genetic risk factors for TBI and TBI-related disorders in this review, as well as the investigation into personalized therapies for these high-risk individuals.

Source link: https://europepmc.org/article/MED/35259824


Urolithin A alleviates blood-brain barrier disruption and attenuates neuronal apoptosis following traumatic brain injury in mice.

However, the effect of traumatic brain injury remains unclear. We established adult C57BL/6J mouse models of traumatic brain injury in this research by controlled cortical exposure and then intraperitoneally administered UA. These findings show that UA may be a candidate for the treatment of traumatic brain injury, and that neuroprotective actions may be aided by blocking the PI3K/Akt/mTOR and Akt/IKK/NFB signaling pathways, thereby reducing neuroinflammation and increasing autophagy.

Source link: https://europepmc.org/article/MED/35142690


Essential role of MALAT1 in reducing traumatic brain injury.

Metastasis-associated lung adenocarcinoma transcript 1 was first reported to be closely linked to lung tumor metastasis by encouraging angiogenesis as a long-coding RNA. To investigate MALAT1's role in traumatic brain injury, we created mouse models of controlled cortical damage and cell models of oxygen-glucose deprivation mimicing traumatic brain injury in vitro and in vivo. Assays reported a valid enhancer of zeste homolog 2 as a downstream cause of MALAT1 in endothelial cells, Bioinformatic experiments and RNA pull-down assays.

Source link: https://europepmc.org/article/MED/35017438


Integrating Human and Nonhuman Primate Data to Estimate Human Tolerances for Traumatic Brain Injury.

Traumatic brain injury is responsible for a significant amount of the injuries resulting from motor vehicle accidents, falls, and sports accidents. In this report, we introduced a new method to establish human injury tolerance levels using an integrated database of reconstructed football effects, subinjurious human volunteer records, and nonhuman primate data. Using tissue-level metrics established using harmonized species-specific finite element brain models, human tolerance levels were determined. The estimated human brain tolerances for mild and severe TBI were estimated and presented in the form of injury risk curves based on selected tissue-level and kinematics-based injury outcomes.

Source link: https://europepmc.org/article/MED/34897386


Diffusion Tensor Imaging Reveals Elevated Diffusivity of White Matter Microstructure that is Independently Associated with Long-Term Outcome after Mild Traumatic Brain Injury: A TRACK-TBI Study.

The DTI literature on single-center studies has contradictory findings regarding the immediate effects of mTBI on WM microstructure and their prognostic significance. This larger-scale multicenter DTI research was designed to determine how acute mTBI affects WM microstructure over time and how early WM changes influence long-term outcomes. A total of 391 acute mTBI patients aged 17-60 years were included and monitored at two weeks and six months postinjury, according to TRACK-TBI, a cohort study at eleven U. S. level 1 trauma centers. mTBI, MD, and RD were both elevated and FA was lower in FA in mTBI versus FC at both two weeks and six months postinjury in both two weeks and six months of cerebral hemispheres, with AD, MD, and RD being higher, while FA was lower in mTBI and RD during the majority of major WM tracts. DTI is one of the leading imaging biomarkers of dynamic WM microstructural shifts after mTBI that have utility for patient selection and treatment response in clinical trials.

Source link: https://europepmc.org/article/MED/35579949


Evidence of traumatic brain injury in headbutting bovids.

Traumatic brain injury is a leading cause of neurologic impairment and death that is still poorly understood. We investigated the risk of brain injury after headbutting in two combative bovid species by determining neuromorphology and neuropathology by immunohistochemistry and stereological quantification. By high-resolution MRI, muskoxen and bighorn sheep's brains were analyzed by high-resolution MRI and processed histologically for signs of TBI. Phosphorylated tau protein, a TBI biomarker present in the cerebrospinal fluid and in neurodegenerative lesions, was used to check potential cellular consequences of chronic or acute TBI. In the bighorn sheep, Tau-immunoreactive lesions were unusual. In addition, microglia and astrocytes showed no grouping around tau-immunoreactive cells in either species. Our preliminary findings reveal that muskoxen and other headbutting bovids suffer from persistent or acute brain injury, and that the males' thicker skulls may shield them to a certain degree.

Source link: https://europepmc.org/article/MED/35579705


A Bayesian MultiLayer Record Linkage Procedure to Analyze PostAcute Care Recovery of Patients with Traumatic Brain Injury.

Understanding the correlations between injury severity and post-acute care for patients with a traumatic brain injury is critical to improving care. In the absence of unique identifiers, record linkage services identify patients across data sets. Patients are a natural grouping scheme for health care because only records that have been treated by the same hospital can show the same patient. To determine the relationship between TBI patients' injury severity and postacute care recovery, we use this method to combine a trauma registry with Medicare claims.

Source link: https://europepmc.org/article/MED/35579386


Photosensitivity Is Associated with Chronic Pain following Traumatic Brain Injury.

Individuals with a history of traumatic brain injury reported an elevated risk of chronic pain. Following TBI, photosensitivity is also a common chronic illness related to TBI and is also widespread among other forms of chronic pain. Based on their Neurobehavioral Symptom Inventory results, the TBI group was divided into 120 symptomatic TBI patients and 113 asymptomatic TBI participants. Participants in the s-TBI program scored significantly higher on self-reported chronic pain measures than those in a-TBI and no-TBI settings, as well as the Symptom Impact Questionnaire Revised and the Michigan Body Map. Despite differences in chronic pain reports, groups maintained similar pressure-pain thresholds. These findings reveal that photosensitivity is linked to self-reported chronic pain and disability in people with persistent TBI symptomatology. Since TBI, photosensitivity could also be used as a simple, more accurate indicator of high-impact chronic pain after TBI.

Source link: https://europepmc.org/article/MED/35373595

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions