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Traumatic Brain Injury - Wiley Online Library

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Last Updated: 18 May 2022

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Impaired mechanotransduction of small cerebral arteries after traumatic brain injury. Role of arachidonic acid pathway dysfunction

The brain's healthy functioning needs precise autoregulation of cerebral blood flow, which is in part facilitated by pressure and flow dependent vaping mechanisms. Traumatic brain injury is common around the world, resulting in brain diseases that cause elevated morbidity and mortality. We hypothesized that TBI damages the authoreregulating mechanisms, specifically the pressure and flow effects of isolated rat middle cerebral arteries consstrictions. Methods TBI was introduced in an anaesthetized rats by weight drop model, and then MCAs were isolated and transferred to a pressure-flow chamber. After TBI, the TP receptor antagonist U46619 triggered substantial constrictions of MCA from intact rats, which were also reduced significantly. We believe that autoregulatory vasomotor pathways play a role in TBI-related human brain disorders such as headaches, brain barrier disruption, brain edema, Alzheimer's disease, and cardiovascular dementia.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.0R725


The pathological progression of repetitive and mild traumatic brain injury in mice

We employed a clinically correct closed-head impact model of engineered rotational acceleration that encourages free rotation of the head on impact caused by an air-compressed piston. Our results point to a novel role for PRMT7 in the disease progression, as shown by the temporal decrease in protein expression post-rmTBI. In our model of mild and repetitive TBI, we measured diffuse axonal injury, leading to increased silver deposition throughout the brain, which is similar to human pathology. We next measured PRMT7 protein levels that had been decreased in the cortex and hippocampus 7 days post-rmTBI. In the cortex 1day post-rmTBI, relative PRMT7 mRNA levels were raised. In addition, mitochondrial fission and fusion were investigated by testing DRP1 and OPA1, and our findings revealed significant rise in DRP1 protein expression 1,3,7 days post rmTBI.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.L7441


Traumatic brain injury in a Drosophila upregulates nitric oxide synthase associated with increased acute behavioral deficits and decreased survival time

Increased GFP production is reported with an elevated Drosophila nitric oxide synthase expression increase. We developed a modified high impact trauma device on NOSGAL4 > UAS2xEGFP flies, where upregulation of Drosophila nitric oxide synthase expression is connected to higher GFP values. TBI from the HIT device was administered to ten flies at different angles, including assessments of acute neurological function, locomotor activity, and brain dNOS levels, twenty-four hours mortality, and survival. HIT angle and sex are also a factor in dNOS expression.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.R2562


Increased Neurovascular Vulnerability to Mild Traumatic Brain Injury in a Mouse Model of Marfan Syndrome

Our results indicate that 6 million old Fbn1+/+ mice have reduced PCA blood flow, cracked PCA wall thickness, increased BBB permeability, and improved NSS scores as compared to 6M-old WT mice, which is similar to 12 million old WT mice. In 6M old Fbn1+/ mice, a precursor to age-matched WT mice, the preliminary investigation into iba1 staining for microglia, a supported assessment of neuroinflammation, shows increased microglial activation in 6M-old Fbn1+/ mice. When testing vulnerability to mild TBI, use of midline fluid percussion injury in 6 million old WT and Fbn1+/> mice, where Fbn1+/ mice required reduced pressure to induce mTBI righting reflex times, the researchers were unable to investigate slight TBI. Using this novel technique of a Marfan Syndrome mouse model that isolates cerebrovascular aging allows for the mechanistic investigation of potential Fbn1 downstream pathways, which may be a therapeutic target for prevention and treatment of post-concussive disorders.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.R4245


Serum from rats subjected to traumatic brain injury and hemorrhagic shock induces profound endothelial barrier dysfunction

Traumatic brain injury has been attributed to the development of indirect acute respiratory distress syndrome (IAPR). We investigated the correlation between TBI and hemorrhagic shock in a rat model on the pulmonary endothelial cell barrier dysfunction, a key feature of ARDs, to explore potential correlations between TBI and ARDS development. Methods The adult male rat polytrauma model consisted of controlled cortical shock induced by blood withdrawal and hemorrhage shock induced by blood withdrawal. Measurement of transendothelial electrical resistance using the electrical cell impedance sensor and visualization of fluorescent tracer penetration into EC monolayer using XPerT assay were used to determine transendothelial cell culture's barrier properties. Both thrombin inhibitor and thrombin receptor antagonist attenuated serum-induced TER decline early in the early stage of CCI-HS serum disruption, but not impact TER decline at later time points. Pulmonary EC adherens junction complexes tested by immunostaining with VECadherin antibody have shown significant decrease in expression of EC junctional protein, VECadherin, and disassembly of peripheral EC adherens junction complexes monitored by immunostaining with VECadherin antibodies. While thrombin PAR1 signaling has been cited as a cause of acute EC permeability rise in CCIHS serum, the determining factor determining long-term EC barrier disruption in CCI's model remains to be determined.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.R4669


Steroid profiling in brain and plasma of adult zebra finches following traumatic brain injury

Traumatic brain injury is a significant health issue and a leading cause of death. In adult male and female zebra finches, we investigated the effects of TBI on local neurosteroid levels around the site of injury and in plasma. An increase in E2 was also present in plasma three days after injury, with elevated levels of 17 estradiol, estrone, and testosterone were found near injured brain tissue three days after the injury. These findings, when combined, reveal that TBI alters neurosteroid levels and are consistent with studies showing that neurosteroids provide neuroprotection following injury.

Source link: https://onlinelibrary.wiley.com/doi/10.1111/jne.13151


Down‐phase auditory stimulation is not able to counteract pharmacologically or physiologically increased sleep depth in traumatic brain injury rats

Modulation of wave activity, either by pharmacological sleep augmentation or sleep restriction, as well as a dramatic reduction of diffuse axonal injury in traumatic brain injury rats, has been attributed to increased posttraumatic cognition and reduced diffuse axonal injury. In our rat model of traumatic brain injury, we investigated the possibility of down-phase targeted auditory stimulation of slow waves and determined its comparative modulatory performance in comparison to the previously used slow-wave activity modulators. Therefore, the use and effectiveness of auditory stimulation as a standalone therapeutic approach in the context of traumatic brain injury warrants further investigation.

Source link: https://onlinelibrary.wiley.com/doi/10.1111/jsr.13615


Center of mass and anatomical coordinate system definition for sheep head kinematics, with application to ovine models of traumatic brain injury

The location, magnitude, and duration of head acceleration during the injury exposure can all influence the pathological results of a traumatic brain injury, as well as diffuse axonal injury. To properly identify the head kinematics after an injury exposure, and therefore a comparison with human head kinematics, anatomical coordinate systems with an origin at the head or brain center of mass production are required, as well as axes that correspond to the ovine Frankfort plane equivalent. Using the Hounsfield unit-mass density relationship, three dimensional models of ten merino sheep heads were constructed from computed tomography photos, as well as a previously announced sheep head coordinate system.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/jnr.25049

* 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