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https://www.readbyqxmd.com/read/29774773/mir-711-induced-down-regulation-of-angiopoietin-1-mediates-neuronal-cell-death
#1
Boris Sabirzhanov, Alan Faden, Taryn Aubrecht, Rebecca Henry, Ethan Glaser, Bogdan A Stoica
Angiopoietin-1 (Ang-1) is a well-known endothelial growth factor but its effects on neurons have yet to be elucidated. We show that Ang-1 is rapidly down-regulated in the injured brain after controlled cortical impact (CCI), a mouse experimental TBI model and in etoposide-induced neuronal apoptosis in vitro. Ang-1 treatment inhibits etoposide-induced up-regulation of pro-apoptotic Bcl-2 family members Noxa, Puma, Bim, and Bax; reduces markers of caspase-dependent (cytochrome c release/caspase activation) and caspase-independent (apoptosis-inducing factor release) pathways; and limits neuronal cell death...
May 18, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29771818/suppressed-acoustic-startle-response-in-traumatic-brain-injury-masks-post-traumatic-stress-disorder-hyper-responsivity
#2
Grant M Liska, Jea-Young Lee, Kaya Xu, Paul R Sanberg, Cesario V Borlongan
An exaggerated acoustic startle reflex (ASR) is a clinical indicator of anxiety disorders, such as post-traumatic stress disorder (PTSD). Given the prevalence of PTSD following traumatic brain injury (TBI), we studied the effects of TBI on ASR. Adult Sprague Dawley rats exposed to moderate controlled cortical impact injury model of TBI displayed suppression of ASR intensity and sensitivity. As patients with PTSD have been shown to display hyperactive startle responses, the present discrepant observation of TBI-induced suppression of ASR has clinical implications, in that the reduced, instead of elevated, startle response in patients with comorbid TBI/PTSD could be owing to a masking effect of TBI...
May 16, 2018: Neuroreport
https://www.readbyqxmd.com/read/29768974/brain-phospholipid-precursors-administered-post-injury-reduce-tissue-damage-and-improve-neurological-outcome-in-experimental-traumatic-brain-injury
#3
Orli Thau-Zuchman, Rita Noutel Gomes, Simon Christopher Dyall, Meirion Davis, John V Priestley, Martine Groenendijk, Martijn DE Wilde, Jordi Lopez-Tremoleda, Adina T Michael-Titus
Traumatic brain injury (TBI) leads to cellular loss, destabilisation of membranes, disruption of synapses and altered brain connectivity, and increased risk of neurodegenerative disease. A significant and long-lasting decrease in phospholipids (PL), essential membrane constituents, has recently been reported in plasma and brain tissue, in human and experimental TBI. We hypothesised that supporting PL synthesis post-injury could improve outcome after TBI. We tested this hypothesis using a multi-nutrient combination designed to support the biosynthesis of phospholipids and available for clinical use...
May 17, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29768967/interleukin-1-receptor-1-deletion-in-focal-and-diffuse-experimental-traumatic-brain-injury-in-mice
#4
Joon Yong Chung, Nicolas Krapp, Limin Wu, Sevda Lule, Lauren McAllister, William Edmiston Iii, Samantha Martin, Emily Levy, Tanya Songtachalert, John Sherwood, Erin Buckley, Bharat Sanders, Saef Izzy, Suzanne Hickman, Shuzhen Guo, Josephine Lok, Joseph El Khoury, Eng Lo, David Kaplan, Michael Whalen
Important differences in the biology of focal and diffuse traumatic brain injury (TBI) subtypes may result in unique pathophysiological responses to shared molecular mechanisms. Interleukin-1 (IL-1) signaling has been tested as a potential therapeutic target in preclinical models of cerebral contusion and diffuse TBI, and in a phase II clinical trial, but no published studies have examined IL-1 signaling in an impact/acceleration closed head injury (CHI) model. We hypothesized that genetic deletion of IL-1 receptor-1 (IL-1R1 KO) would be beneficial in focal (contusion) and CHI in mice...
May 17, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29764720/altered-somatosensory-processing-in-parkinson-s-disease-and-modulation-by-dopaminergic-medications
#5
Aimee J Nelson, Tasnuva Hoque, Carolyn Gunraj, Robert Chen
BACKGROUND: Somatosensory abnormalities contribute to the pathophysiology of Parkinson's disease (PD). The goal of this study was to identify abnormalities in the tactile-evoked activation of the somatosensory and motor cortices in PD, and in a sensorimotor circuit that traverses both of these cortical loci. The second goal was to investigate the impact of dopaminergic medication on these measures. METHODS: Individuals with PD (n = 10, age 61 ± 8 years) and aged-matched controls (n = 11, age 52...
May 7, 2018: Parkinsonism & related Disorders
https://www.readbyqxmd.com/read/29764289/divergent-induction-of-branched-chain-aminotransferases-and-phosphorylation-of-branched-chain-keto-acid-dehydrogenase-is-a-potential-mechanism-coupling-bcka-mediated-astrocyte-activation-to-bcaa-depletion-mediated-cognitive-deficit-after-tbi
#6
Guoqiang Xing, Ming Ren, Ajay Verma
Deficient branched chain amino acids (BCAAs) are implicated in cognitive dysfunction after traumatic brain injury (TBI). The mechanism remains unknown. BCAAs are catabolized by neuron-specific cytosolic and astrocyte-specific mitochondrial branched chain aminotransferases (BCATc, BCATm) to generate glutamate and branched-chain keto-acids (BCKAs) that are metabolized via the mitochondrial branched-chain-keto-acid dehydrogenase (BCKD) whose activity is regulated by its phosphorylation state. BCKD phosphorylation by BCKD kinase (BCKDK) inactivates BCKD and cause neuro-cognitive dysfunction, whereas de-phosphorylation by specific phosphatase restores BCKD activity...
May 15, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29762232/modified-exosomes-reduce-apoptosis-and-ameliorate-neural-deficits-induced-by-traumatic-brain-injury
#7
Bo Wang, Shuangshuang Han
Apoptosis contributes to the pathogenesis of traumatic brain injury (TBI). Engineered exosomes incorporated with therapeutic nuclear acids have been explored for gene therapy for human diseases. The current study sought to investigate the effect of modified exosome-containing plasmids expressing B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X-protein (Bax) shRNA on apoptosis and neural functions after TBI. C57BL/6J mice were subjected to controlled cortical impact injury and were treated with the modified exosomes...
May 11, 2018: ASAIO Journal: a Peer-reviewed Journal of the American Society for Artificial Internal Organs
https://www.readbyqxmd.com/read/29758954/the-use-of-transcranial-magnetic-stimulation-to-evaluate-cortical-excitability-of-lower-limb-musculature-challenges-and-opportunities
#8
Trisha M Kesar, James W Stinear, Steven L Wolf
Neuroplasticity is a fundamental yet relatively unexplored process that can impact rehabilitation of lower extremity (LE) movements. Transcranial magnetic stimulation (TMS) has gained widespread application as a non-invasive brain stimulation technique for evaluating neuroplasticity of the corticospinal pathway. However, a majority of TMS studies have been performed on hand muscles, with a paucity of TMS investigations focused on LE muscles. This perspective review paper proposes that there are unique methodological challenges associated with using TMS to evaluate corticospinal excitability of lower limb muscles...
May 5, 2018: Restorative Neurology and Neuroscience
https://www.readbyqxmd.com/read/29750986/associations-of-functional-connectivity-and-walking-performance-in-multiple-sclerosis
#9
Rachel E Bollaert, Kyle Poe, Elizabeth A Hubbard, Robert W Motl, Lara A Pilutti, Curtis L Johnson, Bradley P Sutton
BACKGROUND: Persons with multiple sclerosis (MS) often demonstrate impaired walking performance, and neuroimaging methods such as resting state functional connectivity (RSFC) may support a link between central nervous system damage and disruptions in walking. OBJECTIVES: This study examined associations between RSFC in cortical networks and walking performance in persons with MS. METHODS: 29 persons with MS underwent 3-T brain magnetic resonance imaging (MRI) and we computed RSFC among 68 Gy matter regions of interest in the brain...
May 8, 2018: Neuropsychologia
https://www.readbyqxmd.com/read/29747570/ketamine-exacerbates-cortical-neuroapoptosis-under-hyperoxic-conditions-by-upregulating-expression-of-the-n-methyl-d-aspartate-receptor-subunit-nr1-in-the-developing-rat-brain
#10
Changyi Wu, Jun Wang, Xiangyang Guo, Ying Zhang
BACKGROUND: Ketamine and hyperoxia are widely used in obstetric and pediatric settings. Either ketamine or hyperoxia has been reported to cause neuroapoptosis in the developing brain, and ketamine-induced neuronal apoptosis may involve a compensatory upregulation of the N-methyl-D-aspartate (NMDA) receptor NR1 subunit. This study investigated the impact of ketamine administration under hyperoxic conditions on cortical neuroapoptosis and NR1 subunit expression in the infant rat brain. METHODS: Male, 7-day-old rats were randomly allocated to four groups: control, ketamine, hyperoxia, and ketamine + hyperoxia (n = 18 per group)...
May 10, 2018: BMC Anesthesiology
https://www.readbyqxmd.com/read/29745374/lesion-volume-estimation-from-tbi-mri
#11
O V Sanjay Sarma, Martha Betancur, Ramana Pidaparti, L Karumbaiah
Traumatic brain injury (TBI) is a major problem affecting millions of people around the world every year. Usually, TBI results from any direct or indirect physical impact, sudden jerks, or blunt impacts to the head, leading to damage to the brain. Current research in TBI is focused on analyzing the biological and behavioral states of patients prone to such injuries. This paper presents a technique applied on MRI images in estimation of lesion volumes in brain tissues of traumatic brain-injured laboratory rats that were subjected to controlled cortical impacts...
2018: Progress in advanced computing and intelligent engineering: proceedings of ICACIE 2016
https://www.readbyqxmd.com/read/29743575/delayed-and-progressive-damages-to-juvenile-mice-after-moderate-traumatic-brain-injury
#12
Shu Zhao, Xiaoting Wang, Xiang Gao, Jinhui Chen
Symptoms are commonly more severe in pediatric traumatic brain injury (TBI) patients than in young adult TBI patients. To understand the mechanism, juvenile mice received a controlled cortical impact (CCI) injury at moderate level. Tissue lesion and cell death were measured and compared to our previous reports on brain injury in the young adult mice that received same level of impact using same injury device. Tissue lesion and cell death in the cortex was much less in the juvenile mouse brain in the first few hours after injury...
May 9, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29743006/unique-properties-associated-with-the-brain-penetrant-iron-chelator-hbed-reveal-remarkable-beneficial-effects-after-brain-trauma
#13
Saher Khalaf, Abdullah Shafique Ahmad, K V D Ranga Chamara, Sylvain Dore
Iron is postulated to contribute to secondary injury after brain trauma through various pathways including oxidative stress and inflammation. Therefore, one goal is to limit iron toxicity by either directly limiting iron activity, or limiting the secondary cascade mediated by iron, therefore rescuing brain damage after trauma. HBED is a unique iron chelator that has the ability to cross the intact blood brain barrier, it has a higher affinity to iron, and it has a longer half-life than most commonly used chelators...
May 10, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29742510/hmgb1-a-box-reverses-brain-edema-and-deterioration-of-neurological-function-in-a-traumatic-brain-injury-mouse-model
#14
Lijun Yang, Feng Wang, Liang Yang, Yunchao Yuan, Yan Chen, Gengshen Zhang, Zhenzeng Fan
BACKGROUND/AIMS: Traumatic brain injury (TBI) is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB), subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1) has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI...
May 8, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29739983/acute-physiology-and-neurologic-outcomes-after-brain-injury-in-scop-phlpp1-ko-mice
#15
Travis C Jackson, C Edward Dixon, Keri Janesko-Feldman, Vincent Vagni, Shawn E Kotermanski, Edwin K Jackson, Patrick M Kochanek
Suprachiasmatic nucleus circadian oscillatory protein (SCOP) (a.k.a. PHLPP1) regulates long-term memory consolidation in the brain. Using a mouse model of controlled cortical impact (CCI) we tested if (1) brain tissue levels of SCOP/PHLPP1 increase after a traumatic brain injury (TBI), and (2) if SCOP/PHLPP1 gene knockout (KO) mice have improved (or worse) neurologic outcomes. Blood chemistry (pH, pCO2 , pO2 , pSO2 , base excess, sodium bicarbonate, and osmolarity) and arterial pressure (MAP) differed in isoflurane anesthetized WT vs...
May 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29738617/sensory-attenuation-of-self-produced-signals-does-not-rely-on-self-specific-motor-predictions
#16
Jakob Kaiser, Simone Schütz-Bosbach
Sensory events produced by ourselves are known to lead to lower neural and perceptual impact than sensory events from other environmental sources. This sensory attenuation is widely assumed to result from control processes that are specific to our own motor actions, potentially helping us to distinguish effects produced by ourselves and others. However, previous research cannot rule out that the putative self-attenuation in fact reflect actor-independent, general predictive mechanisms, which, in direct comparison, just highlight external events due to lower predictability of their onset and thus higher surprise...
May 8, 2018: European Journal of Neuroscience
https://www.readbyqxmd.com/read/29734230/ketamine-alters-hippocampal-cell-proliferation-and-improves-learning-in-mice-after-traumatic-brain-injury
#17
Austin J Peters, Laura E Villasana, Eric Schnell
BACKGROUND: Traumatic brain injury induces cellular proliferation in the hippocampus, which generates new neurons and glial cells during recovery. This process is regulated by N-methyl-D-aspartate-type glutamate receptors, which are inhibited by ketamine. The authors hypothesized that ketamine treatment after traumatic brain injury would reduce hippocampal cell proliferation, leading to worse behavioral outcomes in mice. METHODS: Traumatic brain injury was induced in mice using a controlled cortical impact injury, after which mice (N = 118) received either ketamine or vehicle systemically for 1 week...
April 30, 2018: Anesthesiology
https://www.readbyqxmd.com/read/29722054/pathoarchitectonics-of-the-cerebral-cortex-in-chorea-acanthocytosis-and-hd
#18
Jia Liu, Helmut Heinsen, Lea T Grinberg, Eduardo Alho, Edson Amaro, Carlos A Pasqualucci, Udo Rüb, Kay Seidel, Wilfred den Dunnen, Thomas Arzberger, Christoph Schmitz, Maren C Kiessling, Benedikt Bader, Adrian Danek
AIMS: Quantitative estimation of cortical neurone loss in cases with chorea-acanthocytosis and its impact on laminar composition METHODS: We used unbiased stereological tools to estimate the degree of cortical pathology in serial gallocyanin-stained brain sections through the complete hemispheres of three subjects with genetically verified chorea-acanthocytosis (ChAc) and a range of disease durations. We compared these results with our previous data of five Huntington's disease (HD) and five control cases...
May 2, 2018: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29717625/remote-changes-in-cortical-excitability-after-experimental-tbi-and-functional-reorganization
#19
Derek R Verley, Daneil Torolira, Brandon Pulido, Boris Gutman, Anatol Bragin, Andrew Mayer, Neil G Harris
Although cognitive and behavioral deficits are well known to occur following traumatic brain injury (TBI), motor deficits that occur, even after mild trauma are far less known, yet are equally persistent. This study was aimed at making progress toward determining how the brain reorganizes in response to TBI. We used the adult rat, controlled cortical impact injury model to study the ipsilesional forelimb map evoked by electrical stimulation of the affected limb, as well as the contralesional forelimb map evoked by stimulation of the unaffected limb, both before injury and at 1,2,3 and 4wks after using fMRI...
May 2, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29713797/whole-egg-consumption-and-cortical-bone-in-healthy-children
#20
L M Coheley, J M Kindler, E M Laing, A Oshri, K M Hill Gallant, S J Warden, M Peacock, C M Weaver, R D Lewis
Eggs contain bioactive compounds thought to benefit pediatric bone. This cross-sectional study shows a positive link between childhood egg intake and radius cortical bone. If randomized trials confirm our findings, incorporating eggs into children's diets could have a significant impact in preventing childhood fractures and reducing the risk of osteoporosis. INTRODUCTION: This study examined the relationships between egg consumption and cortical bone in children. METHODS: The cross-sectional study design included 294 9-13-year-old black and white males and females...
April 30, 2018: Osteoporosis International
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