Relevant bibliographies by topics / Glial Fibrillary Acidic Protein (GFAP)

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Academic literature on the topic 'Glial Fibrillary Acidic Protein (GFAP)'

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Published: 14 March 2023

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Journal articles on the topic "Glial Fibrillary Acidic Protein (GFAP)"

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Gravier-Dumonceau, Alice, Roxana Ameli, Veronique Rogemond, Anne Ruiz, Bastien Joubert, Sergio Muñiz-Castrillo, Alberto Vogrig, et al. "Glial Fibrillary Acidic Protein Autoimmunity." Neurology 98, no. 6 (November 19, 2021): e653-e668. http://dx.doi.org/10.1212/wnl.0000000000013087.

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Background and ObjectivesTo report the clinical, biological, and imaging features and clinical course of a French cohort of patients with glial fibrillary acidic protein (GFAP) autoantibodies.MethodsWe retrospectively included all patients who tested positive for GFAP antibodies in the CSF by immunohistochemistry and confirmed by cell-based assay using cells expressing human GFAPα since 2017 from 2 French referral centers.ResultsWe identified 46 patients with GFAP antibodies. Median age at onset was 43 years, and 65% were men. Infectious prodromal symptoms were found in 82%. Other autoimmune diseases were found in 22% of patients, and coexisting neural autoantibodies in 11%. Tumors were present in 24%, and T-cell dysfunction in 23%. The most frequent presentation was subacute meningoencephalitis (85%), with cerebellar dysfunction in 57% of cases. Other clinical presentations included myelitis (30%) and visual (35%) and peripheral nervous system involvement (24%). MRI showed perivascular radial enhancement in 32%, periventricular T2 hyperintensity in 41%, brainstem involvement in 31%, leptomeningeal enhancement in 26%, and reversible splenial lesions in 4 cases. A total of 33 of 40 patients had a monophasic course, associated with a good outcome at last follow-up (Rankin Score ≤2: 89%), despite a severe clinical presentation. Adult and pediatric features are similar. Thirty-two patients were treated with immunotherapy. A total of 11/22 patients showed negative conversion of GFAP antibodies.DiscussionGFAP autoimmunity is mainly associated with acute/subacute meningoencephalomyelitis with prodromal symptoms, for which tumors and T-cell dysfunction are frequent triggers. The majority of patients followed a monophasic course with a good outcome.
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Brenner, Michael. "Glial Fibrillary Acidic Protein (GFAP)." Brain Pathology 4, no. 3 (July 1994): 219–20. http://dx.doi.org/10.1111/j.1750-3639.1994.tb00836.x.

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Yadav, Nidhi, Keshav Mishra, Anil Kumar B. C., Daljit Singh, and Manju Subberwal. "Clinical utility of serum glial fibrillary acidic protein in glial neoplasm." Surgical Neurology International 13 (December 30, 2022): 601. http://dx.doi.org/10.25259/sni_889_2022.

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Background: Glial fibrillary acidic protein (GFAP) is a member of the cytoskeletal protein family and is widely expressed in astroglial and neural stem cells, also in glial tumors such as astrocytoma and Glioblastoma (GBM). Increased GFAP expression and disruption of the blood–brain barrier are the characteristic features of GBM. Higher serum GFAP levels can help differentiate GBM from GBM mimics (such as primary central nervous system lymphoma, metastasis, or demyelinating lesions). Methods: This prospective study was carried out in a tertiary care center in the department of neurosurgery on newly diagnosed glioma patients who underwent surgery from January 2018 to July 2019, excluded patients with history of the previous surgery for glioma, traumatic brain injury, and ischemic or hemorrhagic stroke. The blood sample was obtained at admission before undergoing invasive procedure. Pathological examination of the tumor biopsy sample was carried out using classical hematoxylin-eosin and immunohistochemical staining. All statistical analyses were performed using SPSS version 24.0. Results: The mean preoperative tumor volume was 40 cm3 (range 17.19–65.57 cm3; standard deviation [SD] = 9.99 cm3) which showed 98.25% mean reduction in volume postsurgery (mean tumor volume = 0.7 cm3; SD = 0.19 cm3). Preoperative serum GFAP measurements show higher levels (spearman’s rho coefficient = 0.610 with P = 0.000) with increasing grade of tumor. GFAP levels also demonstrated higher value with increasing preoperative tumor volume. Conclusion: Increasing serum GFAP levels in the preoperative period correlate with higher tumor grade, especially grade III and grade IV tumors. The serum GFAP levels showed relation to tumor volume, both before and after surgery.
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van Asperen, Jessy V., Pierre A. J. T. Robe, and Elly M. Hol. "GFAP Alternative Splicing and the Relevance for Disease – A Focus on Diffuse Gliomas." ASN Neuro 14 (January 2022): 175909142211020. http://dx.doi.org/10.1177/17590914221102065.

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Glial fibrillary acidic protein (GFAP) is an intermediate filament protein that is characteristic for astrocytes and neural stem cells, and their malignant analogues in glioma. Since the discovery of the protein 50 years ago, multiple alternative splice variants of the GFAP gene have been discovered, leading to different GFAP isoforms. In this review, we will describe GFAP isoform expression from gene to protein to network, taking the canonical isoforms GFAPα and the main alternative variant GFAPδ as the starting point. We will discuss the relevance of studying GFAP and its isoforms in disease, with a specific focus on diffuse gliomas.
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Sarthy, Vijay. "Focus on Molecules: Glial fibrillary acidic protein (GFAP)." Experimental Eye Research 84, no. 3 (March 2007): 381–82. http://dx.doi.org/10.1016/j.exer.2005.12.014.

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Chen, W. J., and R. K. Liem. "The endless story of the glial fibrillary acidic protein." Journal of Cell Science 107, no. 8 (August 1, 1994): 2299–311. http://dx.doi.org/10.1242/jcs.107.8.2299.

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All intermediate filament proteins consist of an alpha-helical rod domain flanked by non-helical N-terminal head and C-terminal tail domains. The roles of the non-helical domains of various intermediate filament proteins in the assembly and co-assembly of higher-order filamentous structures have been studied by many groups but with quite contradictory results. Type III intermediate filaments are unique in that they can form homopolymers both in vitro and in vivo. The expression and assembly characteristics of carboxy- and amino-terminal deletion mutants of glial fibrillary acidic protein (GFAP), an astrocyte-specific type III intermediate filament protein, were examined by transient transfections of either vimentin-positive or vimentin-negative variants of human adrenocarcinoma-derived SW13 cell lines. Whereas complete deletion of the C-terminal tail domain of GFAP results in the formation of polymorphic aggregates, both intranuclear and cytoplasmic in self-assembly experiments, efficient co-assembly of these tail-less GFAP mutants with vimentin can be achieved as long as the KLLEGEE sequence at the C-terminal end of the rod domain is preserved. Up to one-fifth of the C-terminal end of the tail domain can be deleted without affecting the capability of GFAP to self-assemble. The highly conserved RDG-containing motif in the tail domain may be important for self-assembly but is not sufficient. The entire head domain seems to be required for self-assembly. All N-terminal deletion mutants of GFAP share the same phenotype of diffuse cytoplasmic staining when expressed in vimentin-negative SW13 cells. Although co-assembly with vimentin can still be achieved with completely head-less GFAP, preservation of some of the head domain greatly enhanced the efficiency. Our results form the basis for further, more detailed mapping of the essential regions in filament assembly of GFAP and other type III IFs.
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Joo, Jae Young, Dallah Yoo, and Tae-Beom Ahn. "Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis." Journal of Movement Disorders 15, no. 1 (January 31, 2022): 66–70. http://dx.doi.org/10.14802/jmd.21115.

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Movement disorders associated with glial fibrillary acidic protein (GFAP) autoantibodies have rarely been reported as ataxia or tremors. A 32-year-old man with headache and fever, initially diagnosed with viral meningoencephalitis, showed gradual improvement with empirical treatment. Two weeks after the illness, he suddenly developed orofacial, tongue, and neck dyskinesia accompanied by oculomotor abnormalities, which developed into severe generalized choreoballism. Brain magnetic resonance imaging (fluid-attenuated inversion recovery) showed signal hyperintensities in the bilateral globus pallidus interna. The clinical picture suggested an acute inflammatory trigger of secondary autoimmune encephalitis. The autoimmune antibody test was positive for GFAP, with the strongest reactivity in the cerebrospinal fluid (CSF) before treatment and decreased reactivity in serial CSF examinations during immunotherapy. Dyskinesia gradually improved to the extent that it could be controlled with only oral medications. This patient presented with parainfectious GFAP meningoencephalitis with distinctive clinical features and imaging findings.
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Lake, Norma, Carole Verdone-Smith, and Seymour Brownstein. "Immunocytochemical localization of taurine and glial fibrillary acidic protein in human optic nerve." Visual Neuroscience 8, no. 3 (March 1992): 251–55. http://dx.doi.org/10.1017/s095252380000290x.

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AbstractTaurine immunoreactivity (IR) in 1 -μm sections of glutaraldehyde-fixed human optic nerve was observed using light microscopy and an antibody raised in rabbit to taurine conjugated to bovine serum albumin. Throughout the nerve, taurine-lR was prominent in glial cells, in their perinuclear regions, and in their numerous branching processes, some of which extended to the pial septa. The peripheral glial mantle (glia limitans) was densely stained, whereas axons and the pial septa showed relatively little or no taurine-IR. Immunoreactivity for glial fibrillary acidic protein (GFAP), an astrocyte-specific marker, was evaluated on adjacent sections. The pattern of GFAP-IR was highly similar to that for taurine, suggesting that a subset of taurine-immunoreactive glial cells are optic nerve astrocytes. To our knowledge, this is the first localization of taurine and GFAP in human optic nerve.
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Deng, Bo, Jingguo Wang, Hai Yu, Lei Jin, Yue Qiu, Xiaoni Liu, Pengyu Wang, Xiang Zhang, and Xiangjun Chen. "Area Postrema Syndrome in Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy." Neurology - Neuroimmunology Neuroinflammation 9, no. 6 (September 26, 2022): e200029. http://dx.doi.org/10.1212/nxi.0000000000200029.

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Background and ObjectivesTo report the frequency of area postrema syndrome (APS) in glial fibrillary acidic protein-immunoglobulin G (GFAP-IgG)–positive patients and emphasize the importance of APS among the phenotypes in autoimmune GFAP astrocytopathy.MethodsEight GFAP-IgG–positive cases with APS were retrospectively identified during 2015–2021. The APS phenotypes were described. A literature review of 8 previously reported cases was also included in analysis.ResultsA total of 8 patients (11%) (1 woman, 7 men; mean age: 52.4 ± 18.4 years) presented with APS in a cohort of 74 GFAP-IgG–positive patients, 3 of whom (4%) had disease onset with APS. All patients had hiccups, and hiccups was the unique symptom of APS in 5 patients. The median time from disease onset to APS occurrence was 2 days (range 0–20), and the mean duration of APS episodes was 23.6 ± 11.4 days. No patient had isolated APS attack. All episodes were completely resolved with a mean duration of 9.3 ± 5.4 days after immunotherapy. APS manifestations of 8 cases in previous studies showed similar features with our cases. In total, coexisting aquaporin-4-IgG was only detected in one of the 16 cases.DiscussionAPS could be an early, but not isolated clinical manifestation of autoimmune GFAP astrocytopathy. Hiccups was the predominant symptom of APS in this disorder. APS attacks of autoimmune GFAP astrocytopathy have good response to immunotherapy.
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Hatfield, James S., Robert P. Skoff, Harry Maisel, Lawrence Eng, and Darell D. Bigner. "The lens epithelium contains glial fibrillary acidic protein (GFAP)." Journal of Neuroimmunology 8 (1985): 347–57. http://dx.doi.org/10.1016/s0165-5728(85)80072-2.

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Dissertations / Theses on the topic "Glial Fibrillary Acidic Protein (GFAP)"

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Malloch, G. D. A. "The development and control of cytoskeletal GFAP assembly in the rat brain and in primary cultures of foetal rat brain cells." Thesis, University of Kent, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332120.

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Steinriede, Anja. "Eingrenzung der Leichenliegezeit mittels immunhistochemischer Untersuchung des Glial-fibrillary-acidic-Protein (GFAP) in Astrocyten." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975443879.

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Aquino, Erika. "Downregulation of glial fibrillary acidic protein (GFAP) by TNF-α : implications for the neurogenic ability of Müller glia." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10054469/.

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Müller glial cells can regenerate the retina in zebrafish throughout life. However, in the damaged adult human retina, upregulation of inflammatory cytokines, including TNF-α, leads to Müller cell gliosis, a hallmark of which is an increase in intermediate filament glial fibrillary acid protein (GFAP) production. However, a subset of these human cells has stem cell characteristics in vitro. This study investigated the role that inflammatory cytokines may play in regulating Müller cell gliosis-associated proteins and the implications this could have on the neurogenic ability of Müller glia in vitro. As determined by gene and protein analysis, culture of the human Müller glial cell line MIO-M1 in the presence of TNF-α, causes downregulation of GFAP expression. Through upregulation of TNF-receptor2 and downstream activation of the NFκB signalling pathway, a cell survival signal is initiated. MIO-M1 cells co-cultured with TNF-α and factors known to induce rod photoreceptor precursor differentiation, showed increased expression of the photoreceptor marker NR2E3. These observations suggest that TNF-α may not inhibit the neurogenic ability of these cells. A retroviral transfection method was developed to overexpress GFAP in MIO-M1 cells using molecular cloning techniques. Overexpression of GFAP resulted in no phenotypic changes as Müller cells maintained their stem cell characteristics. Culturing these transfected cells with TNF-α revealed differential transcriptional regulation of endogenous and exogenous GFAP. This indicates the importance of the GFAP promoter and transcriptional response elements in responding to TNF-α during gliosis. In conclusion, the present study has identified the downregulation of GFAP expression by TNF-α in Müller glial cells as a target that could be further explored to control scarring of the human retina. These observations pave the way for further investigations to promote endogenous regeneration of the adult human retina by Müller glia.
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Desclaux, Mathieu. "Stratégie de régénération axonale dans la moëlle épinière lésée par thérapie génique : inhibition de l'expression des protéines GFAP et Vimentine dans les astrocytes réactionnels par ARN-interférence et suppression de la cicatrice gliale." Paris 6, 2007. http://www.theses.fr/2007PA066534.

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Après une lesion médullaire, les astrocytes réactionnels surexpriment les proteines GFAP et Vimentine, formant ainsi une cicatrice gliale qui constitue un obstacle majeur à la régénération axonale. Les animaux doublement invalidés pour les gènes de la GFAP et de la vimentine présentent, après hémisection de la moelle épinière, une réduction de la cicatrice gliale, une repousse axonale significative ainsi qu’un recouvrement des fonctions locomotrices (Menet et al. 2003). Sur la base de ces résultats, nous avons développé une stratégie de transfert de gènes qui a pour objectif d’inhiber localement l’expression de GFAP et de vimentine par ARN interférence (ARNi) de manière à limiter la formation de cette cicatrice. Dans un premier temps nous avons développé des vecteurs lentiviraux capables de réprimer efficacement l’expression de GFAP et de Vimentine par ARNi in vitro et in vivo. Dans différents modèles cellulaires, nous avons mis en évidence la capacité de ces vecteurs à limiter la formation de cicatrice gliale d’une part, et d’autre part à favoriser la survie neuronale ainsi que la croissance axonale. Enfin, dans un modèle murin d’hémisection médullaire, nous avons montré que l’application de ces vecteurs dans le parenchyme médullaire permet d’améliorer la récupération fonctionnelle et favorise la repousse des fibres sérotoninergiques impliquées dans la locomotion.
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Mignot, Cyril. "Etudes des mécanismes pathologiques en cause dans l'agrégation de la GFAP mutée dans la maladie d'Alexander, une atteinte primaire de l'astrocyte aboutissant à une leucodystrophie." Paris 6, 2007. http://www.theses.fr/2007PA066477.

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La maladie d’Alexander est une maladie neurodégénérative due à des mutations hétérozygotes dans la GFAP, filament intermédiaire majoritaire de l’astrocyte mature, conduisant à la formation d’agrégats La conséquence des mutations de la GFAP sur la formation du cytosquelette astrocytaire, la façon dont les agrégats se forment et l’induction potentielle de processus de défense cellulaires restent à déterminer. Nous avons étudié différentes mutations de la GFAP dans des astrocytes murins sauvages ou dépourvus de GFAP et/ou de vimentine et dans des cellules SW13. Dans les astrocytes, la GFAP mutée produit un réseau ou des agrégats, tandis que la protéine sauvage produit un réseau. La dynamique de la GFAP mutée a été étudiée en vidéo-microscopie. Dans les astrocytes, les agrégats peuvent se déplacer de façon centrifuge et disparaître. Le plus souvent ils se rassemblent près du noyau, ce qui est fréquemment associé à la mort cellulaire et correspond à la formation d’aggresomes. Les petites protéines du stress et le système ubiquitine-protéasome pourraient être impliqués dans la désagrégation, tandis que l’autophagie ne semble pas sollicitée. Nous montrons par ailleurs que l’intégration de GFAP mutée dans un réseau de filament formé par la vimentine prévient la formation des agrégats d’une manière dépendante de la quantité de GFAP exprimée. En conclusion, l’agrégation de la GFAP mutée semble dépendre de la mise en place de mécanismes de défense cellulaire, dont les protéines chaperonnes et le système ubiquitine-protéasome, et de la quantité de GFAP et de vimentine produite par l’astrocyte.
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Hansel, Gisele. "Avaliação de parâmetros neuroquímicos em fatias de hipocampo de rato submetidas à privação de oxigênio e glicose." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/21425.

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Mesmo a isquemia sendo a terceira causa de morte em países industrializados, os mecanismos relacionados a esta doença ainda continuam polêmicos e obscuros. Utilizou-se a técnica de privação de oxigênio e glicose (OGD) em fatias do hipocampo de rato para investigar parâmetros mitocondriais, neurais, astrogliais e metabólicos no período de isquemia e durante o período de reoxigenação. Os resultados mostraram uma diminuição na atividade mitocondrial durante o período isquêmico que foi mantido durante todo o período de reoxigenação. Analisando o sobrenadante destas fatias submetidas à OGD, foi observado que os níveis de LDH, NSE e GFAP se elevaram. Com relação aos níveis de lactato, verificou-se sua diminuição durante todos os períodos. Os níveis de S100B estavam elevados somente durante o período de reoxigenação. Este aumento pode ser tanto um mecanismo de neuroproteção desta proteína frente ao insulto ou ainda uma liberação por dano celular astrocitário. Além disso, foi observado um grande aumento nos níveis de glutamato durante a isquemia e este aumento retornou no período de reoxigenação. Por fim, houve uma diminuição na captação de glutamato somente no período de reoxigenação. Todos estes resultados podem ser conseqüência de uma hiper-estimulação dos receptores glutamatérgicos devido ao insulto isquêmico. Em resumo, nosso estudo mostrou alterações em diversos parâmetros neuroquímicos específicos tanto no período isquêmico quanto na reoxigenação, mostrando que cada tipo celular, reage diferentemente frente ao insulto isquêmico na técnica de OGD in vitro.
Stroke is the third cause of mortality in industrialized countries, and the mechanisms related to this disease are polemic and unclear. Oxygen and glucose deprivation (OGD) in acute rat hippocampal slices was performed to investigate mitochondrial, neural, astroglial and metabolic neurochemical parameters at different ischemic and reoxygenation periods. Results showed the mitochondrial activity decrease due energy failure during ischemic insult and reoxygenation time. In the supernatant medium, LDH, NSE and glutamate levels were increased and the lactate decrease by the lack of energy observed in the ischemic period. Parameters such as GFAP, S100B and glutamate uptake suffered alterations only at the reoxygenation period. These results have shown the vulnerability of neurons facing ischemic insult. Meanwhile, it was also observed a delayed injure of astrocytes only at reoxygenation time, which demonstrate the difference between cell types at OGD. In summary, our finding has shown altered at specific neurochemical parameters in OGD in vitro which features the ischemic episodes and reoxygenation periods.
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Falconer, Robert J. "The effect of electrolytic lesion and neural implants on glial fibrillary acidic protein expression in the rat spinal cord." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28983.

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This thesis assessed the suitability of unilateral, electrolytic lesions as a model of spinal cord damage and repair in the adult rat. This type of lesion resulted acutely in localized damage in the upper motor neuron at the L2-L3 level of the spinal cord. Minimal acute damage to ascending sensory pathways was indicated by preserved somatosensory evoked potentials elicited by stimulation of the tibial nerve. Immediately after lesion generation one of several substrates was injected into the lesion cavity. These substrates were saline buffer, liquid collagen solution, foetal spinal cord cells from 14 day old rat embryos, and a mixture of collagen and E 14 foetal spinal cord cells. The 4 groups were compared for functional recovery over 3 months using the inclined plane test and a Tarlov movement scale. After sacrifice, the tibialis anterior muscles were dissected and weighed to assess atrophy due to lower motor neuron injury. After removing and embedding the spinal cords in paraffin, transverse and longitudinal sections were taken for cytoarchitectural investigation. Cresyl violet was used to indicate Nissl substance, Luxol fast blue stained for myelin and anti - glial fibrillary acidic protein (GFAP) antibody revealed the expression of GFAP in the cord sections. Chronic electrolytic lesions were characterized by the highly variable degree of cavitation, demyelination and macrophage infiltration that was present. There was no significant performance deficit on the inclined plane test in any of the lesioned groups when compared to unoperated animals. The tibialis muscles from all groups were of normal weight, indicating that the lower motor neurons were not significantly damaged by the lesions used. There was, however, a marked decrease in the number of GFAP reactive astrocytes in the lesioned animals when compared to unlesioned controls (P < 0.01, Wilcoxon test). Moreover, this reduction of GFAP - like immunoreactivity was not prevented by implants of foetal neurons, collagen or foetal neurons suspended in collagen. Possible explanations for the reduced GFAP - like immunoreactivity seen in all electrolytically lesioned cords are discussed.
Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
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Nylén, Karin. "Studies of biochemical brain damage markers in patients at a neurointensive care unit /." Göteborg : Institute of Neuroscience and Physiology, Department of Neurology, Göteborg University, 2007. http://hdl.handle.net/2077/4599.

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Zelenika, Diana. "Identification de nouveaux transcrits de la proteine acide des gliofilaments (gfap) et de la proteine basique de la myeline (mbp) dans le systeme nerveux central et dans le systeme immunitaire." Paris 11, 1994. http://www.theses.fr/1994PA11T002.

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Piton, Valérie. "Induction combinée des gènes c-fos, hsp 70 et activation du gène gfap au cours de crises épileptiques provoquées par le soman, un neurotoxique organophosphore." Montpellier 1, 1997. http://www.theses.fr/1997MON1T012.

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Books on the topic "Glial Fibrillary Acidic Protein (GFAP)"

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J, Marangos Paul, Campbell Iain C, and Cohen Robert M, eds. Neuronal and glial proteins: Structure, function, and clinical application. San Diego: Academic Press, 1988.

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Doris, Dahl, ed. Glial cells in the central nervous system and their reaction to injury. Austin, Tex: R.G. Landes, 1994.

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Chen, Wan-Jui. Studies of the glial fibrillary acidic protein: A model for intermediate filament assembly and its function in astrocyte process formation. 1994.

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Marangos, Paul J., and Iain C. Campbell. Neuronal and Glial Proteins: Structure, Function, and Clinical Application (Neurobiological Research). Academic Pr, 1988.

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Marangos, Paul J., and Iain C. Campbell. Neuronal and Glial Proteins: Structure, Function, and Clinical Application (Neurobiological Research). Academic Pr, 1988.

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O’Neill, Brian P., Jeffrey Allen, Mitchell S. Berger, and Rolf-Dieter Kortmann. Astrocytic tumours: pilocytic astrocytoma, pleomorphic xanthoastrocytoma, and subependymal giant cell astrocytoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0002.

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Pilocytic astrocytoma (PA) (World Health Organization (WHO) grade I). A relatively circumscribed, slow-growing, often cystic astrocytoma occurring in children and young adults, histologically characterized by a biphasic pattern with varying proportions of compacted bipolar cells associated with Rosenthal fibres and loose-textured multipolar cells associated with microcysts and eosinophilic granular bodies. Most PAs are localized, macrocystic, and only marginally infiltrative. However some PAs, such as those arising in the optic pathways, are rarely cystic and may have an extensive infiltrative pattern but within a neuroanatomic pathway. Pleomorphic xanthoastrocytoma (PXA) (WHO grade II). An astrocytic neoplasm with a relatively favourable prognosis, typically encountered in children and young adults, with superficial location in the cerebral hemispheres and involvement of the meninges; characteristic histological features include pleomorphic and lipidized cells expressing glial fibrillary acidic protein and often surrounded by a reticulin network as well as eosinophilic granular bodies. Subependymal giant cell astrocytoma (SEGA) (WHO grade I). A benign, slow-growing tumour typically arising in the wall of the lateral ventricles and composed of large ganglioid astrocytes. It is the most common CNS neoplasm in patients with tuberous sclerosis.
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Book chapters on the topic "Glial Fibrillary Acidic Protein (GFAP)"

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Tardy, M., C. Fages, G. Le Prince, B. Rolland, and J. Nunez. "Regulation of the Glial Fibrillary Acidic Protein (GFAP) and of its Encoding mRNA in the Developing Brain and in Cultured Astrocytes." In Molecular Aspects of Development and Aging of the Nervous System, 41–52. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-5876-4_4.

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Kleine, T. O. "Liquor-Glial fibrillary acidic protein." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1925-1.

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Kleine, T. O. "Liquor-Glial fibrillary acidic protein." In Springer Reference Medizin, 1496. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1925.

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Yoshida, Tomokatsu, and Masanori Nakagawa. "Alexander Disease: Role of Glial Fibrillary Acidic Protein." In Tumors of the Central Nervous System, 215–21. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7602-9_22.

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Eng, Douglas L., and Lawrence F. Eng. "Glial Fibrillary Acidic Protein: The Intermediate Filament Protein of Astrocytes." In Advances in Neurobiology, 455–501. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6787-9_20.

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Lake, Norma. "Localization of Taurine and Glial Fibrillary Acidic Protein in Human Optic Nerve Using Immunocytochemical Techniques." In Advances in Experimental Medicine and Biology, 303–7. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3436-5_36.

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Schmidt, D., W. Keil, and D. Harms. "Neuron-Specific Enolase, Protein S-100, Neurofilaments, Glial Fibrillary Acidic Protein and Vimentin as Markers for Cytodifferentiation in Neuroblastoma." In Progress in Surgical Pathology, 33–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-662-12820-6_3.

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Otani, Naoki, H. Nawashiro, N. Nomura, S. Fukui, N. Tsuzuki, S. Ishihara, and K. Shima. "A role of glial fibrillary acidic protein in hippocampal degeneration after cerebral trauma or kainate-induced seizure." In Brain Edema XII, 267–69. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_58.

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Nishiyama, Kazuo, Paul Collodi, Le Sun, and David Barnes. "Leukemia inhibitory factor and related peptides regulate glial fibrillary acidic protein in serum-free mouse embryo (SFME) cells." In Animal Cell Technology: Basic & Applied Aspects, 305–9. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0848-5_46.

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Iwaki, Akiko, Toru Iwaki, Yoshiyuki Sakaki, Ronald K. H. Liem, and James E. Goldman. "Opposite Effects of Cyclic AMP and Cell Density on Expression of αB-Crystallin and Glial Fibrillary Acidic Protein in C-6 Glioma Cells." In Biological Aspects of Brain Tumors, 396–401. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_55.

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Conference papers on the topic "Glial Fibrillary Acidic Protein (GFAP)"

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Leung, Lai Yee, Pamela J. VandeVord, Warren Hardy, Roche De Guzman, King H. Yang, and Albert I. King. "Effects of Short Duration Overpressure on Astrocytes: An In Vitro Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176202.

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Blast wave overpressure from detonations can injure physiological systems ‘silently.’ Experimental and clinical studies have revealed the damaging effects of shock waves on different physiological systems, such as ears, lungs and gastrointestinal tracts [1, 2]. Despite the improved helmet and body armor, many veterans returning from wars suffered from neurological disorders that are being diagnosed as mild traumatic brain injury. Warden (2006) reported that most of these veterans were exposed to blast [3]. In vivo study illustrated neuronal degeneration in the brain after exposure to blast waves [4]. As with many neuronal diseases, blast-induced neuronal injury may be related to microglia and astrocyte activation. However, the underlying mechanism is not clearly understood. This study was aimed at investigating the effects of short duration overpressure on astrocytes, in terms of cell proliferation and mRNA expression of several apoptotic genes and glial fibrillary acidic protein (GFAP).
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Porter, Jason, Adriana Hepner, Manjari Pandey, Philippe Prouet, Felicia Hare, Syed S. Nasir, Madison Boles, Henrik Zetterberg, Kaj Blennow, and Michael Martin. "Abstract 1352: Serum neurofilament light (NfL), glial fibrillary acidic protein (GFAp) and tau protein are possible serum biomarkers for activity of brain metastases and gliomas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1352.

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Porter, Jason, Adriana Hepner, Manjari Pandey, Philippe Prouet, Felicia Hare, Syed S. Nasir, Madison Boles, Henrik Zetterberg, Kaj Blennow, and Michael Martin. "Abstract 1352: Serum neurofilament light (NfL), glial fibrillary acidic protein (GFAp) and tau protein are possible serum biomarkers for activity of brain metastases and gliomas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1352.

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Li, Lulu, Alexander Davidovich, Jennifer Schloss, Uday Chippada, Rene Schloss, Noshir Langrana, and Martin Yarmush. "Control of Neural Lineage Differentiation in an Alginate Encapsulation Microenvironment via Cellular Aggregation." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206496.

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Cell replacement therapies, which utilize renewable stem cell sources, hold tremendous potential to treat a wide range of degenerative diseases. Although many studies have established techniques to successfully differentiate stem cells into different mature cell lineages, their practicality is limited by the lack of control during the differentiation process and low yields of differentiated cells. In order to address these issues, we have previously established a murine embryonic stem cell alginate-poly-L-lysine microencapsulation differentiation system [1]. We demonstrated that ES cell differentiation could be mediated by cell-cell aggregation in the encapsulation microenvironment. We have demonstrated that both cell aggregation and hepatocyte functions, such as urea and albumin secretions, as well as increased expression of cytokeratin 18 and cyp4507a, occur concomitantly with surface E-cadherin expression [2]. In the present studies, we assessed the feasibility of inducing neuronal lineage differentiation in the alginate microenvironment by incorporating soluble inducers, such as retinoic acid, into the permeable microcapsule system. We demonstrated decreased cell aggregation and enhanced neuronal lineage differentiation with the expression of various neuronal specific markers, including neurofilament, A2B5, O1 and glial fibrillary acidic protein (GFAP). In addition, we demonstrated that, by blocking the cell aggregation using anti-E-cadherin antibody, encapsulated cells increased neuronal marker expression at a later stage of the encapsulation, even in the absence of retinoic acid. In conjunction with the mechanical and physical characterizations of the alginate crosslinking network, we show that 2.2% alginate concentration is most conducive to neuronal differentiation from embryonic stem cells in the presence of retinoic acid.
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Shuliatnikova, Tetiana, and Valerii Tumanskyi. "ALTERATIONS OF THE BRAIN GLIAL FIBRILLARY ACIDIC PROTEIN DURING HUMAN LIVER CIRRHOSIS." In DÉBATS SCIENTIFIQUES ET ORIENTATIONS PROSPECTIVES DU DÉVELOPPEMENT SCIENTIFIQUE. La Fedeltà & Plateforme scientifique européenne, 2022. http://dx.doi.org/10.36074/logos-11.11.2022.46.

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Korpela, Sara, Jimmy Sundblom, Henrik Zetterberg, Radu Constantinescu, Per Svenningsson, Martin Paucar Arce, and Valter Niemelä. "D02 Cerebrospinal fluid amyloid beta and glial fibrillary acidic protein concentrations in huntington’s disease." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.33.

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Liao, Chong-Chun, Megha Jhunjhunwala, Li-Han Chung, and Chi-Shuo Chen. "Abstract 2931: The compounding effects of coenzyme q10 and radiation treatment on glial fibrillary acidic protein network of gliomain vitro." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2931.

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Liao, Chong-Chun, Megha Jhunjhunwala, Li-Han Chung, and Chi-Shuo Chen. "Abstract 2931: The compounding effects of coenzyme q10 and radiation treatment on glial fibrillary acidic protein network of gliomain vitro." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2931.

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Reports on the topic "Glial Fibrillary Acidic Protein (GFAP)"

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Tompkins, Christina P., Tracey A. Hamilton, John P. Petrall, and Robert K. Kan. Optimization of Glial Fibrillary Acidic Protein Immunoreactivity in Formalin-fixed, Paraffin-Embedded Guinea Pig Brain Sections. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada443180.

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