scholarly journals THE ROLE OF RECOMBINANT IL-10 ON THE SERUM LEVEL OF TNF-α, ONE HOUR POST TRAUMATIC BRAIN INJURY OF THE WISTAR RAT

2015 ◽  
Vol 4 (1) ◽  
pp. 24
Author(s):  
W. Adhimarta ◽  
A. A. Islam ◽  
S. Maliawan ◽  
G. S. Lowrence ◽  
I. Patellongi
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Serum Level ◽  
Wistar Rat ◽  
Tnf Α ◽  
Post Traumatic

PTSD and Traumatic Brain Injury

2018 ◽  
Author(s):  
Richard A. Bryant
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Stress Responses ◽  
Post Traumatic Stress ◽  
Postconcussive Syndrome ◽  
Post Traumatic ◽  
Explosive Devices ◽  
The Impact ◽  
Distinctive Role

One of the more hotly debated issues in the field of post-traumatic stress disorder (PTSD) is the role of traumatic brain injury (TBI), and particularly mild traumatic brain injury (mTBI). This topic became increasingly the focus of attention in the context of recent wars in Iraq and Afghanistan, where many troops suffered PTSD and mTBIs. Over three-quarters of injuries sustained in these conflicts arose from encounters with explosive devices, and accordingly it was often claimed that the “signature injuries” of the wars in Iraq and Afghanistan were both PTSD and mTBI. Clinicians and researchers have thus given renewed attention to the interplay of these two conditions. This chapter reviews definitional issues of PTSD and mTBI, how PTSD can develop after mTBI, the impact mTBI may have on stress responses, the distinctive role of postconcussive syndrome, and how to manage PTSD following mTBI.

scholarly journals FTO Regulates Microglia-Induced Inflammation by Stabilizing ADAM17 Expression After Experimental Traumatic Brain Injury

2022 ◽  
Author(s):  
Xiangrong Chen ◽  
Jieran Yao ◽  
Yue Chen ◽  
Wenqi Lv ◽  
Yuanxiang Lin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Epigenetic Modification ◽  
Down Regulation ◽  
Neuroinflammatory Response ◽  
Microglial Polarization ◽  
Bv2 Cells ◽  
Tnf Α ◽  
Experimental Traumatic Brain Injury

Abstract Background The neuroinflammatory response mediated by microglial polarization plays an important role in the secondary nerve injury of traumatic brain injury (TBI). The post-transcriptional modification of n6-methyladenosine (m6A) is ubiquitous in the immune response of the central nervous system. The fat mass and obesity (FTO)-related protein can regulate the splicing process of pre-mRNA. However, after experimental traumatic brain injury (TBI), the role of FTO in microglial polarization and the subsequent neuroinflammatory response is still unclear. Methods TBI mice model was established by the Feeney weight-drop method. Neurological severity score, brain water content measurement and Nissl staining were used to detect the role of FTO in microglial polarization and the molecular mechanism of targeted RNA epigenetic modification. In vitro and in vivo experiments were conducted to evaluate microglial polarization and the neuroinflammatory response by down-regulation of FTO expression. The level of m6A modification in M1 activated microglia was detected by qRT-PCR, m6A-MeRIP and m6A high-throughput sequencing. Fluorescent in situ hybridization combined with immunofluorescence imaging were used to detect the epigenetic regulation of ADAM17 mediated by an FTO-m6A-dependent mechanism. Results The expression of FTO was significantly down-regulated in BV2 cells treated with lipopolysaccharide and mice with TBI. Down-regulation of FTO expression increased the level of m6A in M1 microglia at the level of the entire transcriptome. Meanwhile, after FTO interference, M1/M0 phenotype detection experiments revealed the BV2 cells shifted from an M0 to M1 phenotype as the population rate of CD11b+/CD86+ increased and secretion of pro-inflammatory cytokines was enhanced. Methylated RNA immunoprecipitation assay showed that the m6A peaks located in the ADAM17 and TNF-α genes increased. Taken together, the results indicated that FTO can affect the transcription modification of ADAM17 and the expression of the downstream TNF-α/NF-kB pathway. In turn, ADAM17 can block the M1-phenotypic transition of microglia driven by FTO-m6A modification. Conclusions The down-regulation of FTO expression leads to the abnormally high expression of ADAM17 in microglia. The activation of microglia and neuroinflammatory response regulated by FTO-related m6A modification play an important role in the early pro-inflammatory process of TBI secondary injury.

The Role of Self-Discrepancy Theory in Understanding Post–Traumatic Brain Injury Affective Disorders

2005 ◽  
Vol 20 (6) ◽  
pp. 527-543 ◽  
Author(s):  
Joshua B. Cantor ◽  
Teresa A. Ashman ◽  
Michael E. Schwartz ◽  
Wayne A. Gordon ◽  
Mary R. Hibbard ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Affective Disorders ◽  
Discrepancy Theory ◽  
Post Traumatic ◽  
Self Discrepancy

scholarly journals Incidence of post-traumatic pneumonia in poly-traumatized patients: identifying the role of traumatic brain injury and chest trauma

2019 ◽  
Vol 46 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Martijn Hofman ◽  
Hagen Andruszkow ◽  
Philipp Kobbe ◽  
Martijn Poeze ◽  
Frank Hildebrand
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Chest Trauma ◽  
Post Traumatic

scholarly journals Examining the role of astrogliosis and JNK signaling in post-traumatic epilepsy

2022 ◽  
Vol 37 (1) ◽  
Author(s):  
Coulter Small ◽  
Abeer Dagra ◽  
Melanie Martinez ◽  
Eric Williams ◽  
Brandon Lucke-Wold
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Kainic Acid ◽  
Seizure Activity ◽  
Moderate Traumatic Brain Injury ◽  
Post Traumatic ◽  
Post Traumatic Epilepsy ◽  
Acid Administration ◽  
Traumatic Epilepsy

Abstract Objective Post-traumatic epilepsy is a devastating complication of traumatic brain injury that has no targeted pharmacological therapy. Previous literature has explored the role of the c-Jun N-terminal kinase (JNK) pathway in epilepsy and the creation of epileptogenic foci by reactive astrogliosis; however, the relationship between reactive astrogliosis and the c-Jun N-terminal kinase signaling pathway in the development of post-traumatic epilepsy has not been thoroughly examined. Methods Four experimental groups, consisting of c57/b16 male mice, were examined: (1) control, (2) traumatic brain injury of graded severity (mild, moderate, severe), (3) sub-convulsive kainic acid alone without traumatic brain injury (15 mg/kg i.p.), and (4) sub-convulsive kainic acid administered 72 h after moderate traumatic brain injury. Modified Racine scale from 1 to 72 h and total beam breaks at 72 h were used to assess seizure activity. Immunohistochemistry and western blot were utilized to examine astrogliosis (GFAP), microglia activation (IBA-1), and phosphorylated JNK in prefrontal cortex samples collected from the contracoup side at 72 h post-injury. Results Astrogliosis, measured by GFAP, was increased after traumatic brain injury and increased commensurately based on the degree of injury. Mice with traumatic brain injury demonstrated a four-fold increase in phosphorylated JNK: p < 0.001. Sub-convulsive kainic acid administration did not increase seizure activity nor phosphorylation of JNK in mice without traumatic brain injury; however, sub-convulsive kainic acid administration in mice with moderate traumatic brain injury did increase phosphorylated JNK. Seizure activity was worse in mice, with traumatic brain injury, administered kainic acid than mice administered kainic acid. Conclusions Reactive astrocytes may have dysfunctional glutamate regulation causing an increase in phosphorylated JNK after kainic acid administration. Future studies exploring the effects of JNK inhibition on post-traumatic epilepsy are recommended.

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