scholarly journals Using Autopsy Brain Tissue to Study Alcohol-Related Brain Damage in the Genomic Age

2013 ◽  
Vol 38 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Greg T. Sutherland ◽  
Donna Sheedy ◽  
Jillian J. Kril
Keyword(s):  
Brain Tissue ◽  
Brain Damage ◽  
Autopsy Brain Tissue

scholarly journals Establishment of an Experimental Intracerebral Haemorrhage Model for Mass Effect Research using a Thermo-sensitive Hydrogel

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yuhua Gong ◽  
Yuping Gong ◽  
Zongkun Hou ◽  
Tingwang Guo ◽  
Jia Deng ◽  
...  
Keyword(s):  
Cell Death ◽  
Brain Tissue ◽  
Brain Damage ◽  
Intracerebral Haemorrhage ◽  
Brain Oedema ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mass Effect ◽  
Iron Deposition ◽  
Mass Effects

Abstract The mechanical response of brain tissue closely relates to cerebral blood flow and brain diseases. During intracerebral haemorrhage (ICH), a mass effect occurs during the initial bleeding and results in significant tissue deformation. However, fewer studies have focused on the brain damage mechanisms and treatment approaches associated with mass effects compared to the secondary brain injuries after ICH, which may be a result of the absence of acceptable animal models mimicking a mass effect. Thus, a thermo-sensitive poly (N-isopropylacrylamide) (PNIPAM) hydrogel was synthesized and injected into the rat brain to establish an ICH model for mass effect research. The PNIPAM hydrogel or autologous blood was injected to establish an ICH animal model, and the space-occupying volumes, brain tissue elasticity, brain oedema, neuronal cell death, iron deposition and behavioural recovery were evaluated. The lower critical solution temperature of PNIPAM hydrogel was 32 °C, and the PNIPAM hydrogel had a rough surface with similar topography and pore structure to a blood clot. Furthermore, the ICH model animals who received an injection of PNIPAM and blood produced similar lesion volumes, elasticity changes and mechanically activated ion channel piezo-2 upregulation in brain tissue. Meanwhile, slight iron deposition, neuronal cell death and brain oedema were observed in the PNIPAM hydrogel model compared to the blood model. In addition, the PNIPAM hydrogel showed good biocompatibility and stability in vivo via subcutaneous implantation. Our findings show that PNIPAM hydrogel cerebral infusion can form a mass effect similar to haematoma and minimize the interference of blood, and the establishment of a mass effect ICH model is beneficial for understanding the mechanism of primary brain injury and the role of mass effects in secondary brain damage after ICH.

P1-213: Telomere length in autopsy brain tissue in dementia

2010 ◽  
Vol 6 ◽  
pp. S235-S236
Author(s):  
Lawrence S. Honig ◽  
Min-Suk Kang ◽  
Lorraine Clark ◽  
Joseph H. Lee
Keyword(s):  
Telomere Length ◽  
Brain Tissue ◽  
Autopsy Brain Tissue

Aflatoxins in the autopsy brain tissue of children in Nigeria

1995 ◽  
Vol 132 (1) ◽  
pp. 35-38 ◽  
Author(s):  
O. A. Oyelami ◽  
S. M. Maxwell ◽  
K. A. Adelusola ◽  
T. A. Aladekoma ◽  
A. O. Oyelese
Keyword(s):  
Brain Tissue ◽  
Autopsy Brain Tissue

scholarly journals The Competitive NMDA Antagonist CGP 40116 Permanently Reduces Brain Damage after Middle Cerebral Artery Occlusion in Rats

1995 ◽  
Vol 15 (4) ◽  
pp. 602-610 ◽  
Author(s):  
Dirk Sauer ◽  
Edgar Weber ◽  
Guido Lüönd ◽  
Fernando Da Silva ◽  
Peter R. Allegrini
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Brain Tissue ◽  
Brain Damage ◽  
Analysis Of Variance ◽  
Cerebral Artery ◽  
Nmda Antagonist ◽  
Histological Evaluation ◽  
Mca Occlusion ◽  
Cgp 40116

In this study we evaluated the effect of the competitive N-methyl-d-aspartate (NMDA) antagonist d-(E)-4-(3-phosphonoprop-2-enyl)piperazine-2-carboxylic acid (CGP 40116) on both early (2 days) and late (28 days) ischemic brain damage in a rodent model of focal cerebral ischemia by means of magnetic resonance imaging (MRI) and conventional histology. Immediately after occlusion of the left middle cerebral artery (MCA), rats received either CGP 40116 (20 mg/kg i.p.) or isotonic saline. Two MRI scans were performed in each animal 2 and 28 days after MCA occlusion. After the second scan, rats were perfusion fixed for histological evaluation. The volume of lesioned brain tissue as determined by MRI or histology was calculated from the damaged area in single sections and the distance between them. CGP 40116 reduced acute infarct volume as measured by MRI 2 days after MCA occlusion by 44% (p < 0.05, analysis of variance). After 28 days the lesion detected by MRI was still significantly smaller in the drug-treated animals. This finding was confirmed by the histological analysis showing a 64% reduction in the volume of brain atrophy in the CGP 40116 group (p < 0.05, analysis of variance). There was a good correlation between the MRI data and the results of the histological evaluation ( r = 0.9). Our results indicate that (a) the competitive NMDA antagonist CGP 40116 permanently protects brain tissue from the consequences of cerebral ischemia in a rat model for human stroke and (b) early and late pathological changes can be accurately measured by MRI.

Determination of mercury and lead levels in autopsy brain tissue samples

2009 ◽  
Vol 189 ◽  
pp. S220 ◽  
Author(s):  
Seda Kaya ◽  
Vugar Aliyev ◽  
Servet B. Iritas ◽  
Tülin Soylemezoglu
Keyword(s):  
Brain Tissue ◽  
Tissue Samples ◽  
Autopsy Brain Tissue ◽  
Lead Levels

scholarly journals Neuromechanical characterization of brain damage in response to head impact and pathological changes

2020 ◽  
Keyword(s):  
Brain Tumor ◽  
Brain Tissue ◽  
Brain Damage ◽  
Damage Mechanics ◽  
Continuum Damage Mechanics ◽  
Head Impact ◽  
The Body ◽  
Large Strains ◽  
Modeling Tools ◽  
Initial Anisotropy

Traumatic injuries to the central nervous system (brain and spinal cord) have received special attention because of their devastating socio-economical cost. Functional and morphological damage of brain is the most intricate phenomenon in the body. It is the major cause of disability and death. The paper involves constitutive modeling and computational investigations towards an understanding the mechanical and functional failure of brain due to the traumatic (head impact) and pathological (brain tumor) events within the framework of continuum damage mechanics of brain. Development of brain damage has been analyzed at the organ scale with the whole brain, tissue scale with white and gray tissue, and cellular scale with an individual neuron. The mechanisms of neurodamage growth have been specified in response to head impact and brain tumor. Swelling due to electrical activity of nervous cells under electrophysiological impairments, and elastoplastic deformation and creep under mechanical loading of the brain have been analyzed. The constitutive laws of neuromechanical behavior at large strains have been developed, and tension-compression asymmetry, as well as, initial anisotropy of brain tissue was taken into account. Implementation details of the integrated neuromechanical constitutive model including the Hodgkin-Huxley model for voltage into ABAQUS, ANSYS and in-house developed software have been considered in a form of the computer-based structural modeling tools for analyzing stress distributions over time in healthy and diseased brains, for neurodamage analysis and for lifetime predictions of diseased brains. The outcome of this analysis will be how the neuromechanical simulations applied to the head impact and brain tumor therapies may assist medical specialists with their decisions during planning and application of medical surgeries.

scholarly journals CX3CL1 Recruits NK Cells Into the Central Nervous System and Aggravates Brain Injury of Mice Caused by Angiostrongylus cantonensis Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Rong Zhang ◽  
Tingting Miao ◽  
Min Qin ◽  
Chengsi Zhao ◽  
Wei Wang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Flow Cytometry ◽  
Nervous System ◽  
Brain Injury ◽  
Nk Cells ◽  
Brain Tissue ◽  
Brain Damage ◽  
Adoptive Transfer ◽  
Angiostrongylus Cantonensis ◽  
The Brain

BackgroundAngiostrongylus cantonensis (A. cantonensis), is a food-borne zoonotic parasite that can cause central nervous system (CNS) injury characterized by eosinophilic meningitis. However, the pathogenesis of angiostrongylosis remains elusive. Natural killer cells (NK cells) are unique innate lymphocytes important in early defense against pathogens. The aim of this study was to investigate the role of NK cells in A. cantonensis infection and to elucidate the key factors that recruit NK cells into the CNS.MethodsMouse model of A. cantonensis infection was established by intragastric administration of third-stage larvae. The expression of cytokines and chemokines at gene and protein levels was analyzed by qRT-PCR and ELISA. Distribution of NK cells was observed by immunohistochemistry and flow cytometry. NK cell-mediated cytotoxicity against YAC-1 cells was detected by LDH release assay. The ability of NK cells to secrete cytokines was determined by intracellular flow cytometry and ELISA. Depletion and adoptive transfer of NK cells in vivo was induced by tail vein injection of anti-asialo GM1 rabbit serum and purified splenic NK cells, respectively. CX3CL1 neutralization experiment was performed by intraperitoneal injection of anti-CX3CL1 rat IgG.ResultsThe infiltration of NK cells in the CNS of A. cantonensis-infected mice was observed from 14 dpi and reached the peak on 18 and 22 dpi. Compared with uninfected splenic NK cells, the CNS-infiltrated NK cells of infected mice showed enhanced cytotoxicity and increased IFN-γ and TNF-α production ability. Depletion of NK cells alleviated brain injury, whereas adoptive transfer of NK cells exacerbated brain damage in A. cantonensis-infected mice. The expression of CX3CL1 in the brain tissue and its receptor CX3CR1 on the CNS-infiltrated NK cells were both elevated after A. cantonensis infection. CX3CL1 neutralization reduced the percentage and absolute number of the CNS-infiltrated NK cells and relieved brain damage caused by A. cantonensis infection.ConclusionsOur results demonstrate that the up-regulated CX3CL1 in the brain tissue recruits NK cells into the CNS and aggravates brain damage caused by A. cantonensis infection. The findings improve the understanding of the pathogenesis of angiostrongyliasis and expand the therapeutic intervention in CNS disease.

Significant Role of microRNA-182-5p in Neonatal Hypoxic-Ischemic Injury and Related Mechanism

2020 ◽  
Vol 10 (5) ◽  
pp. 654-661
Author(s):  
Qin Wang ◽  
Ting Wang
Keyword(s):  
Cell Viability ◽  
Brain Tissue ◽  
Brain Damage ◽  
Rat Model ◽  
Target Gene ◽  
Luciferase Reporter ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Qrt Pcr ◽  
The Brain

The purpose of current study was to explore the role and mechanism of microRNA-182-5p (miR182-5p) in neonatal hypoxic ischemic brain damage (HIBD). First, we established a hypoxic-ischemic (HI) rat model and assessed the neurological function of the rats using the Zea Longa score. Then, the level of miR-182-5p in brain tissue of neonatal rats was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Findings revealed that miR-182-5p was significantly down-regulated in the brain tissue of HI rat model. Next, we studied the target gene of miR-182-5p by using TargetScan and dual luciferase reporter assay. Results showed that CASP2 was a direct target gene of miR-182-5p, and the level of CASP2 was significantly up-regulated in the brain tissue of HI rat model. Immediately thereafter, we established an oxygen and glucose deprivation (OGD) cell model of primary cortical neurons, and demonstrated the changes of miR182-5p in cells treated with OGD by qRT-PCR. Finally, to determine the function of miR-182-5p in OGD subjected neuronal cells, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and flow cytometry (FCM) assays were used to study cell viability and apoptosis. The study found that compared with the OGD group, miR-182-5p mimic significantly increased nerve cell viability, reduced cell apoptosis and decreased cleaved-Caspase3/7/8 protein expression, however, all these changes were significantly reversed by overexpression of the CASP2 gene. Taken together, miR-182-5p might protect the nerve cells from ischemia and hypoxia by targeting CASP2, thereby playing a protective role in hypoxic ischemic encephalopathy, which might be a new effective target for neonatal hypoxic ischemic brain damage treatment.

scholarly journals Biochemical and molecular studies using human autopsy brain tissue

2003 ◽  
Vol 85 (3) ◽  
pp. 543-562 ◽  
Author(s):  
Matthew R. Hynd ◽  
Joanne M. Lewohl ◽  
Heather L. Scott ◽  
Peter R. Dodd
Keyword(s):  
Brain Tissue ◽  
Molecular Studies ◽  
Autopsy Brain Tissue ◽  
Human Autopsy
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