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https://www.readbyqxmd.com/read/29150743/differential-response-of-neural-cells-to-trauma-induced-swelling-in-vitro
#1
A R Jayakumar, M Taherian, K S Panickar, N Shamaladevi, M E Rodriguez, B G Price, M D Norenberg
Brain edema and the associated increase in intracranial pressure are major consequences of traumatic brain injury (TBI) that accounts for most early deaths after TBI. We recently showed that acute severe trauma to cultured astrocytes results in cell swelling. We further examined whether trauma induces cell swelling in neurons and microglia. We found that severe trauma also caused cell swelling in cultured neurons, whereas no swelling was observed in microglia. While severe trauma caused cell swelling in both astrocytes and neurons, mild trauma to astrocytes, neurons, and microglia failed to cell swelling...
November 17, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/29138458/low-intensity-pulsed-ultrasound-improves-behavioral-and-histological-outcomes-after-experimental-traumatic-brain-injury
#2
Wei-Shen Su, Chun-Hu Wu, Szu-Fu Chen, Feng-Yi Yang
The purpose of this study was to investigate the neuroprotective effects of low-intensity pulsed ultrasound (LIPUS) on behavioral and histological outcomes in a mouse model of traumatic brain injury (TBI). Mice subjected to controlled cortical impact injury were treated with LIPUS in the injured region daily for a period of 4 weeks. The effects of LIPUS on edema were observed by MR imaging in the mouse brain at 1 and 4 days following TBI. Brain water content, blood-brain barrier permeability, histology analysis, and behavioral studies were performed to assess the effects of LIPUS...
November 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29113926/the-role-of-microrna-in-traumatic-brain-injury
#3
REVIEW
Yuan-Bo Pan, Zhao-Liang Sun, Dong-Fu Feng
Traumatic brain injury (TBI) is a public health problem that causes high mortality and disability worldwide. Secondary brain damage from this type of injury may cause brain edema, blood-brain barrier destruction, and neurological dysfunction. MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene expression at the post-transcriptional level and play vital roles in maintaining and regulating physiological function. Notably, studies suggest that miRNA levels are altered in the cerebral cortex and hippocampus of rats and mice after TBI...
November 4, 2017: Neuroscience
https://www.readbyqxmd.com/read/29079445/selective-activation-of-cannabinoid-receptor-2-reduces-neuroinflammation-after-traumatic-brain-injury-via-alternative-macrophage-polarization
#4
Molly Braun, Zenab T Khan, Mohammad B Khan, Manish Kumar, Ayobami Ward, Bhagelu R Achyut, Ali S Arbab, David C Hess, Md Nasrul Hoda, Babak Baban, Krishnan M Dhandapani, Kumar Vaibhav
Inflammation is an important mediator of secondary neurological injury after traumatic brain injury (TBI). Endocannabinoids, endogenously produced arachidonate based lipids, have recently emerged as powerful anti-inflammatory compounds, yet the molecular and cellular mechanisms underlying these effects are poorly defined. Endocannabinoids are physiological ligands for two known cannabinoid receptors, CB1R and CB2R. In the present study, we hypothesized that selective activation of CB2R attenuates neuroinflammation and reduces neurovascular injury after TBI...
October 24, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29067455/hyperbaric-oxygen-alleviates-the-activation-of-nlrp%C3%A2-3%C3%A2-inflammasomes-in-traumatic-brain-injury
#5
Huihui Qian, Qinghe Li, Woda Shi
Growing evidence has demonstrated that the nucleotide‑binding oligomerization domain‑like receptor family pyrin domain containing 3 (NLRP‑3) inflammasome‑mediated inflammatory pathways have been involved in the secondary injury of traumatic brain injury (TBI). In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP‑3 inflammasome pathway following TBI. Following the evaluation of motor deficits and brain edema, the therapeutic effects of HBO on interleukin (IL)‑1β and IL‑18 expression were assessed, as well as NLRP‑3 inflammasome activation following TBI...
October 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29061477/effect-of-hypothermia-on-apoptosis-in-traumatic-brain-injury-and-hemorrhagic-shock-model
#6
Oğuz Eroğlu, Turgut Deniz, Üçler Kisa, Pınar Atasoy, Kuzey Aydinuraz
INTRODUCTION: The neuroprotective mechanisms of therapeutic hypothermia against trauma-related injury have not been fully understood yet. In this study, we aimed to investigate the effects of therapeutic hypothermia on biochemical and histopathological markers of apoptosis using Traumatic brain injury (TBI) and hemorrhagic shock (HS) model. METHODS: A total of 50 male albino-wistar rats were divided into five groups: Group isolated TBI, Group NT (HT+HS+normothermia), Group MH (HT+HS+mild hypothermia), Group MoH (HT+HS+moderate hypothermia) and Group C (control)...
September 28, 2017: Injury
https://www.readbyqxmd.com/read/29054447/deletion-ofmst1-attenuates-neuronal-loss-andimproves-neurological-impairment-inarat-model-oftraumatic-brain-injury
#7
Di Li, Haibo Ni, Qin Rui, Rong Gao, Gang Chen
Neuronal cell death following traumatic brain injury (TBI) is a considerable contributor to neurological deficits. In our work, we explored the functions of Mammalian STE20-like kinase-1 (Mst1), a apoptosis-promoting kinase and aslo a pivotal bridgebuilder of apoptotic signaling, in the etiopathogenesis of an experimental rat model of TBI. We found that the phosphorylation level of Mst1 in injured area was significantly increased after TBI. Furthermore, we discovered that inhibition of Mst1 phosphorylation can effectively reduce neuronal cell death by inhibiting the activation of caspase 3 and suppressing the damage of DNA during TBI...
October 17, 2017: Brain Research
https://www.readbyqxmd.com/read/29049053/treatment-options-for-posttraumatic-epilepsy
#8
Lara L Zimmermann, Ryan M Martin, Fady Girgis
PURPOSE OF REVIEW: Posttraumatic seizures (PTS) and posttraumatic epilepsy (PTE) are common and debilitating consequences of traumatic brain injury (TBI). Early PTS result in secondary brain injury by raising intracranial pressure and worsening cerebral edema and metabolic crisis. PTE is a localization-related epilepsy strongly associated with TBI severity, but risk factors for PTE and epileptogenesis are incompletely understood and are active areas of research. Medical management of PTS in adults and children is reviewed...
December 2017: Current Opinion in Neurology
https://www.readbyqxmd.com/read/29028768/hydrogen-gas-treatment-improves-the-neurological-outcome-after-traumatic-brain-injury-via-increasing-mir-21-expression
#9
Lu Wang, Chongfa Zhao, Shuang Wu, Guanghui Xiao, Xin Zhuge, Ping Lei, Keliang Xie
Hydrogen gas (H2) exerts a beneficial effect against traumatic brain injury (TBI). miR-21 is one of the most highly expressed members of small non-coding microRNA family in mammalian cells. miR-21 can improve the neurological outcome after TBI. In the present study, we investigated whether H2 treatment could improve the neurological outcome after TBI via increasing miR-21 expression. TBI was induced by controlled cortical impact (CCI) in rats. H2 treatment was given by exposure to 2% H2 from 30 minutes to 5 hours after TBI operation...
October 12, 2017: Shock
https://www.readbyqxmd.com/read/29026665/lasting-bilateral-mydriasis-after-traumatic-brain-injury-may-not-always-be-a-lost-case
#10
Alkinoos Athanasiou, Ioannis Balogiannis, Ioannis Magras
BACKGROUND: Lasting bilateral mydriasis and absence of pupillary light reflex following severe traumatic brain injury (TBI) are considered signs of irreversible brainstem damage and have been strongly associated with poor outcome. CASE DESCRIPTION: A young female patient presented with severe TBI, contusions, and diffuse brain edema. She was initially treated medically, but developed delayed secondary refractory intracranial hypertension and bilaterally dilated, non-reactive pupils for 12 h...
2017: Surgical Neurology International
https://www.readbyqxmd.com/read/28993515/nonclassical-monocytes-mediate-secondary-injury-neurocognitive-outcome-and-neutrophil-infiltration-after-traumatic-brain-injury
#11
Hadijat M Makinde, Carla M Cuda, Talia B Just, Harris R Perlman, Steven J Schwulst
Traumatic brain injury (TBI) results in rapid recruitment of leukocytes into the injured brain. Monocytes constitute a significant proportion of the initial infiltrate and have the potential to propagate secondary brain injury or generate an environment of repair and regeneration. Monocytes are a diverse population of cells (classical, intermediate, and nonclassical) with distinct functions, however, the recruitment order of these subpopulations to the injured brain largely remains unknown. Thus, we examined which monocyte subpopulations are required for the generation of early inflammatory infiltrate within the injured brain, and whether their depletion attenuates secondary injury or neurocognitive outcome...
November 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28963372/lack-of-mitochondrial-ferritin-aggravated-neurological-deficits-via-enhancing-oxidative-stress-in-a-traumatic-brain-injury-murine-model
#12
Ligang Wang, Libo Wang, Zhibo Dai, Pei Wu, Huaizhang Shi, Shiguang Zhao
Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured...
December 22, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28938628/mir-144-promotes-%C3%AE-amyloid-accumulation-induced-cognitive-impairments-by-targeting-adam10-following-traumatic-brain-injury
#13
Liqian Sun, Manman Zhao, Jingbo Zhang, Aihua Liu, Wenjun Ji, Youxiang Li, Xinjian Yang, Zhongxue Wu
The dysregulation expression of microRNAs (miRNAs) including miR-144, has been widely documented in TBI. However, little is known about the potential roles of miR-144 in the pathogenesis of TBI. In this study, we investigated the potential effects of miR-144 on cognitive function in vivo and in vitro. The results indicated that inhibition of miR-144 conferred a better neurological outcome after TBI in vivo, as evidenced by reduced lesion volume, alleviated brain edema and increased mNSS, of particular importance, improved cognitive deficits...
August 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/28912751/decreased-secondary-lesion-growth-and-attenuated-immune-response-after-traumatic-brain-injury-in-tlr2-4-mice
#14
Sandro M Krieg, Florian Voigt, Pascal Knuefermann, Carsten Jürgen Kirschning, Nikolaus Plesnila, Florian Ringel
Danger-associated molecular patterns are released by damaged cells and trigger neuroinflammation through activation of non-specific pattern recognition receptors, e.g., toll-like receptors (TLRs). Since the role of TLR2 and 4 after traumatic brain injury (TBI) is still unclear, we examined the outcome and the expression of pro-inflammatory mediators after experimental TBI in Tlr2/4(-/-) and wild-type (WT) mice. Tlr2/4(-/-) and WT mice were subjected to controlled cortical injury and contusion volume and brain edema formation were assessed 24 h thereafter...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28905273/early-to-long-term-alterations-of-cns-barriers-after-traumatic-brain-injury-considerations-for-drug-development
#15
Beatriz Rodriguez-Grande, Aleksandra Ichkova, Sighild Lemarchant, Jerome Badaut
Traumatic brain injury (TBI) is one of the leading causes of death and disability, particularly amongst the young and the elderly. The functions of the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) are strongly impaired after TBI, thus affecting brain homeostasis. Following the primary mechanical injury that characterizes TBI, a secondary injury develops over time, including events such as edema formation, oxidative stress, neuroinflammation, and alterations in paracelullar and transcellular transport...
November 2017: AAPS Journal
https://www.readbyqxmd.com/read/28856566/cold-environment-exacerbates-brain-pathology-and-oxidative-stress-following-traumatic-brain-injuries-potential-therapeutic-effects-of-nanowired-antioxidant-compound-h-290-51
#16
Aruna Sharma, Dafin F Muresanu, José Vicente Lafuente, Per-Ove Sjöquist, Ranjana Patnaik, Z Ryan Tian, Asya Ozkizilcik, Hari S Sharma
The possibility that traumatic brain injury (TBI) occurring in a cold environment exacerbates brain pathology and oxidative stress was examined in our rat model. TBI was inflicted by making a longitudinal incision into the right parietal cerebral cortex (2 mm deep and 4 mm long) in cold-acclimatized rats (5 °C for 3 h daily for 5 weeks) or animals at room temperature under Equithesin anesthesia. TBI in cold-exposed rats exhibited pronounced increase in brain lucigenin (LCG), luminol (LUM), and malondialdehyde (MDA) and marked pronounced decrease in glutathione (GTH) as compared to identical TBI at room temperature...
August 30, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28836291/introducing-the-concept-of-csf-shift-edema-in-traumatic-brain-injury
#17
REVIEW
Iype Cherian, Margarita Beltran, Alessandro Landi, Concetta Alafaci, Fabio Torregrossa, Giovanni Grasso
Brain edema after severe traumatic brain injury (TBI) plays an important role in the outcome and survival of injured patients. It is also one of the main targets in the therapeutic approach in the current clinical practice. To date, the pathophysiology of traumatic brain swelling is complex and, being that it is thought to be mainly cytotoxic and vasogenic in origin, not yet entirely understood. However, based on new understandings of the hydrodynamic aspects of cerebrospinal fluid (CSF), an additional mechanism of brain swelling can be considered...
August 24, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28835703/neuroprotective-effects-of-cgp3466b-on-apoptosis-are-modulated-by-protein-l-isoaspartate-d-aspartate-o-methyltransferase-mst1-pathways-after-traumatic-brain-injury-in-rats
#18
Feng Liang, Ligen Shi, Jingwei Zheng, Sheng Chen, Yangxin Wang, Jianmin Zhang
Neuronal apoptosis chiefly contributes to the cell loss following traumatic brain injury (TBI). CGP3466B is a compound related to the anti-Parkinsonism drug R-(-)-deprenyl. Previous studies have illuminated anti-apoptosis effects of CGP3466B in different cell lines, but the underlying mechanisms have not been fully elucidated. Mammalian sterile 20 (STE20)-like kinase1 (Mst1) is a core component of the Hippo signaling pathway. Protein-L-isoaspartate (D-aspartate) O-methyltransferase (PCMT1) is an enzyme that repairs damaged L-isoaspartyl residues in proteins...
August 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28812113/-pathophysiology-of-intracranial-injuries
#19
REVIEW
D Lahner, G Fritsch
Traumatic brain injury (TBI) constitutes a heterogeneous condition that affects the most complex organ of the human body. It is commonly classified by its location as focal injury (e.g. epidural hematoma) and diffuse injury (e.g. diffuse axonal shearing injury) as well as by primary and secondary tissue injury. Accordingly, direct mechanical force causes the primary insult. The tissue damage occurring afterwards is subsumed under the term secondary brain damage. Some of these processes are overlapping and include in the early phase local cerebral ischemia resulting in excitotoxicity, which together with the triggered neuroinflammatory cascade causes the formation of cerebral edema and ultimately increased intracranial pressure once the intracranial compliance is exhausted...
September 2017: Der Unfallchirurg
https://www.readbyqxmd.com/read/28782716/treatment-with-an-interleukin-1-receptor-antagonist-mitigates-neuroinflammation-and-brain-damage-after-polytrauma
#20
Mujun Sun, Rhys D Brady, David K Wright, Hyun Ah Kim, Shenpeng R Zhang, Christopher G Sobey, Maddison R Johnstone, Terence J O'Brien, Bridgette D Semple, Stuart J McDonald, Sandy R Shultz
Traumatic brain injury (TBI) and long bone fracture are common in polytrauma. This injury combination in mice results in elevated levels of the pro-inflammatory cytokine interleukin-1β (IL-1β) and exacerbated neuropathology when compared to isolated-TBI. Here we examined the effect of treatment with an IL-1 receptor antagonist (IL-1ra) in mice given a TBI and a concomitant tibial fracture (i.e., polytrauma). Adult male C57BL/6 mice were given sham-injuries or polytrauma and treated with saline-vehicle or IL-1ra (100mg/kg)...
August 3, 2017: Brain, Behavior, and Immunity
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