scholarly journals Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Rats

2021 ◽  
Vol 11 (7) ◽  
pp. 889
Author(s):  
Anton D. Filev ◽  
Denis N. Silachev ◽  
Ivan A. Ryzhkov ◽  
Konstantin N. Lapin ◽  
Anastasiya S. Babkina ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Target Genes ◽  
Neural Function ◽  
Stress Genes ◽  
Expression Of Genes ◽  
Delayed Recovery ◽  
The Brain ◽  
Lower Expression

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

scholarly journals Decompressive craniectomy of post-traumatic brain injury: an in silico modelling approach for intracranial hypertension management

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chryso Lambride ◽  
Nicolas Christodoulou ◽  
Anna Michail ◽  
Vasileios Vavourakis ◽  
Triantafyllos Stylianopoulos
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Brain Tissue ◽  
Decompressive Craniectomy ◽  
In Silico ◽  
Pressure Loading ◽  
Post Traumatic ◽  
The Brain

Abstract Traumatic brain injury (TBI) causes brain edema that induces increased intracranial pressure and decreased cerebral perfusion. Decompressive craniectomy has been recommended as a surgical procedure for the management of swollen brain and intracranial hypertension. Proper location and size of a decompressive craniectomy, however, remain controversial and no clinical guidelines are available. Mathematical and computational (in silico) models can predict the optimum geometric conditions and provide insights for the brain mechanical response following a decompressive craniectomy. In this work, we present a finite element model of post-traumatic brain injury and decompressive craniectomy that incorporates a biphasic, nonlinear biomechanical model of the brain. A homogenous pressure is applied in the brain to represent the intracranial pressure loading caused by the tissue swelling and the models calculate the deformations and stresses in the brain as well as the herniated volume of the brain tissue that exits the skull following craniectomy. Simulations for different craniectomy geometries (unilateral, bifrontal and bifrontal with midline bar) and sizes are employed to identify optimal clinical conditions of decompressive craniectomy. The reported results for the herniated volume of the brain tissue as a function of the intracranial pressure loading under a specific geometry and size of craniectomy are exceptionally relevant for decompressive craniectomy planning.

scholarly journals Analysis of the Histopathology, TNF-α of Microglia Cells Expression, NRG-1/erbB Oligodendrocyte, and Ki67/Apoptosis of Dentate Gyrus Rattus novergicus Brain After Acute Traumatic Brain Injury

2017 ◽  
Vol 6 (1) ◽  
pp. 20
Author(s):  
Wibi Riawan ◽  
Putri Fitri Alfiantya ◽  
Oktavia Rahayu Adianingsih ◽  
Zulkarnaen Zulkarnaen ◽  
Alif Fariz Jazmi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Dentate Gyrus ◽  
Brain Tissue ◽  
Microscopic Observation ◽  
Pyramidal Cells ◽  
Adult Brain ◽  
Sprague Dawley ◽  
Tnf Α ◽  
The Brain

Head trauma or traumatic brain injury (TBI) gives most serious impact on the central nervous system. Several experimental models have been established to mimic different pathogenesis characteristics of TBI. The purpose of this study was to determine whether there is evidence of hystopathological lesions in the brain tissue after Marmorou TBI models. This study uses Rattus norvegicus Sprague Dawley strain. Macroscopic and microscopic observations on the brain tissue were done. Macroscopic lesions were observed in the brain. Microscopic observation was performed with Haematoxylin-Eosin (HE) staining and immunohistochemistry on the distribution of microglia cells and pyramidal cells in the cortex. Meanwhile, the distribution of NRG-1/ErbB, proliferation, and apoptosis were observed in the hippocampus. The results of macroscopic observation showed that there were wounds caused by falling loads and vasodilatation. On microscopic observation, the TBI group showed an increase in neutrophils distribution and distribution of activated microglia to produce TNF-α, and decrease in the number of cortical pyramidal cells significantly. The distribution of NRG-1 tended to decrease after exposure of TBI and had no effect on its receptor, erbB. Exposure of TBI appears to lower the activity of neuronal cells proliferation in dentate gyrus (DG) area and significantly increase the number of apoptotic cells. Marmarou model is a physiological model of TBI that spontaneously occurs following a trauma to the head, for example trauma due to an accident. This data can be used as a preliminary data of inflammation and tissue regeneration of disrupted adult brain. Therefore, this research could be used as the basis in the studies of therapeutic agents in the process of neurogenesis of brain cells.Keywords: traumatic brain injury, ERG-1/ErbB, dentate gyrus, Ki67, TNF-a, microglia

scholarly journals Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Einars Kupats ◽  
Gundega Stelfa ◽  
Baiba Zvejniece ◽  
Solveiga Grinberga ◽  
Edijs Vavers ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Aminobutyric Acid ◽  
Drug Candidate ◽  
H2o2 Production ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
The Impact ◽  
The Brain

Altered neuronal Ca2+ homeostasis and mitochondrial dysfunction play a central role in the pathogenesis of traumatic brain injury (TBI). R-Phenibut ((3R)-phenyl-4-aminobutyric acid) is an antagonist of the α2δ subunit of voltage-dependent calcium channels (VDCC) and an agonist of gamma-aminobutyric acid B (GABA-B) receptors. The aim of this study was to evaluate the potential therapeutic effects of R-phenibut following the lateral fluid percussion injury (latFPI) model of TBI in mice and the impact of R- and S-phenibut on mitochondrial functionality in vitro. By determining the bioavailability of R-phenibut in the mouse brain tissue and plasma, we found that R-phenibut (50 mg/kg) reached the brain tissue 15 min after intraperitoneal (i.p.) and peroral (p.o.) injections. The maximal concentration of R-phenibut in the brain tissues was 0.6 μg/g and 0.2 μg/g tissue after i.p. and p.o. administration, respectively. Male Swiss-Webster mice received i.p. injections of R-phenibut at doses of 10 or 50 mg/kg 2 h after TBI and then once daily for 7 days. R-Phenibut treatment at the dose of 50 mg/kg significantly ameliorated functional deficits after TBI on postinjury days 1, 4, and 7. Seven days after TBI, the number of Nissl-stained dark neurons (N-DNs) and interleukin-1beta (IL-1β) expression in the cerebral neocortex in the area of cortical impact were reduced. Moreover, the addition of R- and S-phenibut at a concentration of 0.5 μg/ml inhibited calcium-induced mitochondrial swelling in the brain homogenate and prevented anoxia-reoxygenation-induced increases in mitochondrial H2O2 production and the H2O2/O ratio. Taken together, these results suggest that R-phenibut could serve as a neuroprotective agent and promising drug candidate for treating TBI.

New Insights into Oxidative Damage and Iron Associated Impairment in Traumatic Brain Injury

2020 ◽  
Vol 25 (45) ◽  
pp. 4737-4746
Author(s):  
Nicolas Toro-Urrego ◽  
Liliana F. Turner ◽  
Marco F. Avila-Rodriguez
Keyword(s):  
Reactive Oxygen Species ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Oxidative Damage ◽  
Brain Tissue ◽  
Reactive Oxygen ◽  
Iron Chelators ◽  
Oxygen Species ◽  
Underlying Mechanisms ◽  
The Brain

: Traumatic Brain Injury is considered one of the most prevalent causes of death around the world; more than seventy millions of individuals sustain the condition per year. The consequences of traumatic brain injury on brain tissue are complex and multifactorial, hence, the current palliative treatments are limited to improve patients’ quality of life. The subsequent hemorrhage caused by trauma and the ongoing oxidative process generated by biochemical disturbances in the in the brain tissue may increase iron levels and reactive oxygen species. The relationship between oxidative damage and the traumatic brain injury is well known, for that reason, diminishing factors that potentiate the production of reactive oxygen species have a promissory therapeutic use. Iron chelators are molecules capable of scavenging the oxidative damage from the brain tissue and are currently in use for ironoverload- derived diseases. : Here, we show an updated overview of the underlying mechanisms of the oxidative damage after traumatic brain injury. Later, we introduced the potential use of iron chelators as neuroprotective compounds for traumatic brain injury, highlighting the action mechanisms of iron chelators and their current clinical applications.

Gallic acid improved behavior, brain electrophysiology, and inflammation in a rat model of traumatic brain injury

2015 ◽  
Vol 93 (8) ◽  
pp. 687-694 ◽  
Author(s):  
Alireza Sarkaki ◽  
Yaghoub Farbood ◽  
Mohammad Kazem Gharib-Naseri ◽  
Mohammad Badavi ◽  
Mohammad Taghi Mansouri ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Gallic Acid ◽  
Brain Tissue ◽  
Proinflammatory Cytokines ◽  
Repeated Measures ◽  
Long Term Potentiation ◽  
Tissue Levels ◽  
Tnf Α ◽  
The Brain

Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. In the clinic it is essential to limit the development of cognitive impairment after TBI. In this study, the effects of gallic acid (GA; 100 mg/kg, per oral, from 7 days before to 2 days after TBI induction) on neurological score, passive avoidance memory, long-term potentiation (LTP) deficits, and levels of proinflammatory cytokines including interleukin-1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) in the brain have been evaluated. Brain injury was induced following Marmarou’s method. Data were analyzed by one-way and repeated measures ANOVA followed by Tukey’s post-hoc test. The results indicated that memory was significantly impaired (p < 0.001) in the group treated with TBI + vehicle, together with deterioration of the hippocampal LTP and increased brain tissue levels of IL-1β, IL-6, and TNF-α. GA treatment significantly improved memory and LTP in the TBI rats. The brain tissue levels of IL-1β, IL-6, and TNF-α were significantly reduced (p < 0.001) in the group treated with GA. The results suggest that GA has neuroprotective properties against TBI-induced behavioral, electrophysiological, and inflammatory disorders, probably via the decrease of cerebral proinflammatory cytokines.

Effect of Cerebral Vasculatures on the Mechanical Response of Brain Tissue: A Preliminary Study

2000 ◽  
Author(s):  
Kiyoshi Omori ◽  
Liying Zhang ◽  
King H. Yang ◽  
Albert I. King
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Mechanical Response ◽  
Clinical Symptoms ◽  
Anatomical Structure ◽  
Causal Mechanism ◽  
Injury Biomechanics ◽  
Preliminary Study ◽  
The Brain

Abstract Traumatic brain injury (TBI) constitutes a significant portion of all injuries occurring as a result of automotive, motorcycle and sports related injuries. Over the years, a large amount of literature has been devoted to an increased understanding of clinical symptoms, pathological evidence and injury biomechanics for such injuries. However, the precise causal mechanism, which accounts for complex mechanical interactions and responses in an anatomical structure as complex as the brain, is not fully understood.

scholarly journals Prognostic significance of translocator protein in the brain tissue following traumatic brain injury

2021 ◽  
Author(s):  
Qing Bao ◽  
Xuesong Yuan ◽  
Xiaoxing Bian ◽  
Wenfeng Wei ◽  
Peng Jin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Brain Tissue ◽  
Characteristic Curve ◽  
Prognostic Significance ◽  
Translocator Protein ◽  
Specificity And Sensitivity ◽  
Unit Increase ◽  
The Brain

Abstract Background The study aimed to measure the expression of translocator protein (TSPO) in brain tissue following traumatic brain injury (TBI) and to determine whether TSPO can predict outcomes. Methods TBI patients requiring emergent craniectomy and removing of intracranial hematoma were recruited from Wujin Hospital Affiliated with Jiangsu University between January 2018 and May 2020. TBI patients were divided into unfavorable and favorable groups according to GOS score. The TSPO in brain samples was analyzed by western blot and immunocytochemistry. Results The western blot and immunocytochemistry showed that the TSPO in the unfavorable group was higher than that in the favorable group. Double immunofluorescence staining exhibited that the percentage of TSPO positive cells in IBA1 and GFAP positive cells was 45.2 ± 3.1% and 3.5 ± 0.6% respectively. After adjusting for age, sex, CT, ICP and GCS, we found each 1-unit increase in TSPO was associated with 40% higher occurrence of unfavorable outcome (OR = 1.4, 95% CI 0.4–5.6). The area under the receiver operating characteristic curve (AUC), specificity, and sensitivity of TSPO was 0.87, 76.7%, 88.2% respectively. Conclusion Our study demonstrated that higher TSPO was associated with higher occurrence of unfavorable outcomes.

Comparison of Brain Tissue Material Finite Element Models Based on Threshold for Traumatic Brain Injury

2016 ◽  
Author(s):  
Ashkan Eslaminejad ◽  
Hesam Sarvghad-Moghaddam ◽  
Asghar Rezaei ◽  
Mariusz Ziejewski ◽  
Ghodrat Karami
Keyword(s):  
Traumatic Brain Injury ◽  
Finite Element ◽  
Brain Injury ◽  
Dynamic Response ◽  
Brain Tissue ◽  
Head Model ◽  
Fe Modeling ◽  
Material Models ◽  
The Brain ◽  
Tissue Material

Blast traumatic brain injury (bTBI) may happen due to sudden blast and high-frequency loads. Due to the moral issues and the burden of experimental approaches, using computational methods such as finite element analysis (FEA) can be effective. Several finite element studies have focused on the effects of TBI to anticipate and understand the brain dynamic response. One of the most important factors in every FEA study of bTBI is the accurate modeling of brain tissue material properties. The main goal of this study is a comparison of different brain tissue constitutive models to understand the dynamic response of brain under an identical blast load. The multi-material FE modeling of the human head has several limitations such as its complexity and consequently high computational costs. Therefore, a spherical head model is modeled which suggests more straightforward observation/understanding of the FE modeling of skull (solid), CSF (fluid), and the brain tissue. Three different material models are considered for the brain tissue, namely hyperelastic, viscoelastic, and hyperviscoelastic. Brain dynamic responses are studied in terms of the head kinematics (linear acceleration), intracranial pressure (ICP), shear stress, and maximum mechanical strain. Our results showed that the hyperelastic model predicts larger ICP and shear than other constitutive brain tissue models. However, all material models predicted similar shear strain and head accelerations.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

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