Academic literature on the topic 'GFAP biomarker'

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Journal articles on the topic "GFAP biomarker"

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Huss, André, Ahmed Abdelhak, Benjamin Mayer, Hayrettin Tumani, Hans-Peter Müller, Katharina Althaus, Jan Kassubek, et al. "Association of Serum GFAP with Functional and Neurocognitive Outcome in Sporadic Small Vessel Disease." Biomedicines 10, no. 8 (August 2, 2022): 1869. http://dx.doi.org/10.3390/biomedicines10081869.

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Cerebrospinal fluid (CSF) and serum biomarkers are critical for clinical decision making in neurological diseases. In cerebral small vessel disease (CSVD), white matter hyperintensities (WMH) are an important neuroimaging biomarker, but more blood-based biomarkers capturing different aspects of CSVD pathology are needed. In 42 sporadic CSVD patients, we prospectively analysed WMH on magnetic resonance imaging (MRI) and the biomarkers neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), chitinase3-like protein 1 (CHI3L1), Tau and Aβ1-42 in CSF and NfL and GFAP in serum. GFAP and CHI3L1 expression was studied in post-mortem brain tissue in additional cases. CSVD cases with higher serum NfL and GFAP levels had a higher modified Rankin Scale (mRS) and NIHSS score and lower CSF Aβ1-42 levels, whereas the CSF NfL and CHI3L1 levels were positively correlated with the WMH load. Moreover, the serum GFAP levels significantly correlated with the neurocognitive functions. Pathological analyses in CSVD revealed a high density of GFAP-immunoreactive fibrillary astrocytic processes in the periventricular white matter and clusters of CHI3L1-immunoreactive astrocytes in the basal ganglia and thalamus. Thus, besides NfL, serum GFAP is a highly promising fluid biomarker of sporadic CSVD, because it does not only correlate with the clinical severity but also correlates with the cognitive function in patients.
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Högel, Heidi, Eero Rissanen, Christian Barro, Markus Matilainen, Marjo Nylund, Jens Kuhle, and Laura Airas. "Serum glial fibrillary acidic protein correlates with multiple sclerosis disease severity." Multiple Sclerosis Journal 26, no. 2 (December 20, 2018): 210–19. http://dx.doi.org/10.1177/1352458518819380.

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Background: Cerebrospinal fluid (CSF) levels of two soluble biomarkers, glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL), have been shown to associate with multiple sclerosis (MS) disease progression. Now, both biomarkers can be detected reliably in serum, and importantly, their serum levels correlate well with their CSF levels. Objective: To evaluate the usability of serum GFAP measurement as a biomarker of progressive disease and disease severity in MS. Methods: Clinical course, Expanded Disability Status Scale (EDSS), disease duration, patient age and magnetic resonance imaging (MRI) parameters were reviewed in 79 MS patients in this cross-sectional hospital-based study. Serum samples were collected for measurement of GFAP and NfL concentrations using single molecule array (Simoa) assay. A cohort of healthy controls was evaluated for comparison. Results: Higher serum concentrations of both GFAP and NfL were associated with higher EDSS, older age, longer disease duration, progressive disease course and MRI pathology. Conclusion: Earlier studies have demonstrated that GFAP, unlike NfL, is not increased in association with acute focal inflammation-related nervous system damage. Our work suggests that GFAP serum level associates with disease progression in MS and could potentially serve as an easily measurable biomarker of central nervous system (CNS) pathology related to disease progression in MS.
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Bustamante, Alejandro, Anna Penalba, Cyrille Orset, Leire Azurmendi, Víctor Llombart, Alba Simats, Emili Pecharroman, et al. "Blood Biomarkers to Differentiate Ischemic and Hemorrhagic Strokes." Neurology 96, no. 15 (March 5, 2021): e1928-e1939. http://dx.doi.org/10.1212/wnl.0000000000011742.

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ObjectiveTo validate a panel of blood biomarkers to differentiate between ischemic stroke (IS) and intracerebral hemorrhage (ICH) in patients with suspected stroke.MethodsPatients with suspected stroke admitted within 4.5 hours after onset were enrolled. Blood samples were collected at hospital admission. Glial fibrillary acid protein (GFAP), retinol binding protein 4 (RBP-4), N-terminal proB-type natriuretic peptide (NT-proBNP), and endostatin were measured by immunoassays. Cutoff points were obtained for 100% specificity for IS. A high-sensitivity assay to measure GFAP and rapid point-of-care tests (POCTs) to measure RBP-4 and NT-proBNP were used in subsets of patients. Biomarker panels were evaluated in another cohort of 62 stroke mimics.ResultsA total of 189 patients (154 IS and 35 ICH) were enrolled. Patients with IS had higher RBP-4, NT-proBNP, and endostatin and lower GFAP levels than patients with ICH. The best biomarker combination for the identification of IS was RBP-4+NT-proBNP, which was able to identify 29.7% of patients with IS with 100% specificity. In the subset of patients for whom GFAP was measured with the high-sensitivity assay, RBP-4, NT-proBNP, and GFAP identified 51.5% of patients with IS with 100% specificity. When stroke mimics were included, specificities were reduced to 98.4 and 96.8%, respectively. POCTs of RBP-4 and NT-proBNP showed results similar results to those of conventional ELISAs.ConclusionsA biomarker panel including RBP-4, NT-proBNP, and GFAP provided moderate but potentially useful sensitivity rates at 100% specificity for IS diagnosis. If confirmed in future studies, this strategy might allow prehospital treatment in selected patients.Classification of EvidenceThis study provides Class I evidence that a biomarker panel including RBP-4, NT-proBNP, and GFAP distinguishes IS from ICH with moderate accuracy.
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Halford, Julia, Sean Shen, Kyohei Itamura, Jaclynn Levine, Albert C. Chong, Gregg Czerwieniec, Thomas C. Glenn, et al. "New astroglial injury-defined biomarkers for neurotrauma assessment." Journal of Cerebral Blood Flow & Metabolism 37, no. 10 (August 17, 2017): 3278–99. http://dx.doi.org/10.1177/0271678x17724681.

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Traumatic brain injury (TBI) is an expanding public health epidemic with pathophysiology that is difficult to diagnose and thus treat. TBI biomarkers should assess patients across severities and reveal pathophysiology, but currently, their kinetics and specificity are unclear. No single ideal TBI biomarker exists. We identified new candidates from a TBI CSF proteome by selecting trauma-released, astrocyte-enriched proteins including aldolase C (ALDOC), its 38kD breakdown product (BDP), brain lipid binding protein (BLBP), astrocytic phosphoprotein (PEA15), glutamine synthetase (GS) and new 18-25kD-GFAP-BDPs. Their levels increased over four orders of magnitude in severe TBI CSF. First post-injury week, ALDOC levels were markedly high and stable. Short-lived BLBP and PEA15 related to injury progression. ALDOC, BLBP and PEA15 appeared hyper-acutely and were similarly robust in severe and mild TBI blood; 25kD-GFAP-BDP appeared overnight after TBI and was rarely present after mild TBI. Using a human culture trauma model, we investigated biomarker kinetics. Wounded (mechanoporated) astrocytes released ALDOC, BLBP and PEA15 acutely. Delayed cell death corresponded with GFAP release and proteolysis into small GFAP-BDPs. Associating biomarkers with cellular injury stages produced astroglial injury-defined (AID) biomarkers that facilitate TBI assessment, as neurological deficits are rooted not only in death of CNS cells, but also in their functional compromise.
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Borko, Tyler L., Britney Barrera, Christopher Mizenko, Aurélie Ledreux, Ryan Kammeyer, Alanna Ritchie, Sean Selva, et al. "Examining the Differences in Biomarkers of Neuronal and Glial Injury Between Autoimmune Neurologic Disease Patients and Healthy Controls." Neurology 99, no. 23 Supplement 2 (December 5, 2022): S8—S9. http://dx.doi.org/10.1212/01.wnl.0000903096.36040.1d.

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ObjectiveTo evaluate differences in concentrations of serum-based biomarkers obtained from a screened healthy control (HC) population compared to age and sex matched autoimmune and inflammatory neurologic disease (AIND) patients.BackgroundProtein markers of neuronal and glial injury have become important, minimally invasive biomarkers for understanding the impact of disease in various neurological disorders, including ongoing research into AINDs. Levels of these proteins in healthy individuals remain unclear.Design/MethodsNeurofilament light (NfL), glial fibrillary acidic protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), and total tau (Tau) levels in AIND and HC participants will be compared. Multiple Sclerosis (MS) patients, as inflammatory controls, will be analyzed as well. AIND and HC participant serum samples have been collected to obtain NfL, GFAP, UCH-L1, and Tau protein levels using Quanterix SR-XTM SIMOA. We plan to analyze and compare age and sex matched HC samples to AIND patients for each biomarker, ages ranging from 20-80 years old. Concentrations will be log transformed and analyzed with mixed model regression.ResultsHealthy Controls (130), AIND (255), and newly diagnosed/treatment naïve MS samples (681) have already been collected. Nineteen HC and AIND (includes NMDA, LGI1, TRIM46, CRMP5, MOG, DPPX, GABA-A, GAD-65) participants were analyzed. Preliminary results for HC show mean Nfl (10.3 pg/mL), GFAP (78.9 pg/mL), UCH-L1 (5.65 pg/mL), and Tau (0.53 pg/mL) levels, and for AIND patients mean Nfl (186.48 pg/mL), GFAP (434.92 pg/mL), UCH-L1 (71.38 pg/mL), and Tau (51.85 pg/mL) levels. While ongoing biomarker analysis will be completed with HC that are age and sex matched, the significantly higher levels in AIND patients highlights the importance of creating baseline values in HC to understand these same biomarkers in AIND patients.ConclusionsPreliminary results show NfL and GFAP levels are significantly higher in AIND patients versus HC. Baseline biomarker values are essential for understanding further research in biomarkers related to AIND.
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Ganne, Akshatha, Meenakshisundaram Balasubramaniam, W. Sue T. Griffin, Robert J. Shmookler Reis, and Srinivas Ayyadevara. "Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease." Pharmaceutics 14, no. 7 (June 26, 2022): 1354. http://dx.doi.org/10.3390/pharmaceutics14071354.

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Glial fibrillary acidic protein (GFAP) is an intermediate filament structural protein involved in cytoskeleton assembly and integrity, expressed in high abundance in activated glial cells. GFAP is neuroprotective, as knockout mice are hypersensitive to traumatic brain injury. GFAP in cerebrospinal fluid is a biomarker of Alzheimer’s disease (AD), dementia with Lewy bodies, and frontotemporal dementia (FTD). Here, we present novel evidence that GFAP is markedly overexpressed and differentially phosphorylated in AD hippocampus, especially in AD with the apolipoprotein E [ε4, ε4] genotype, relative to age-matched controls (AMCs). Kinases that phosphorylate GFAP are upregulated in AD relative to AMC. A knockdown of these kinases in SH-SY5Y-APPSw human neuroblastoma cells reduced amyloid accrual and lowered protein aggregation and associated behavioral traits in C. elegans models of polyglutamine aggregation (as observed in Huntington’s disease) and of Alzheimer’s-like amyloid formation. In silico screening of the ChemBridge structural library identified a small molecule, MSR1, with stable and specific binding to GFAP. Both MSR1 exposure and GF AP-specific RNAi knockdown reduce aggregation with remarkably high concordance of aggregate proteins depleted. These data imply that GFAP and its phosphorylation play key roles in neuropathic aggregate accrual and provide valuable new biomarkers, as well as novel therapeutic targets to alleviate, delay, or prevent AD.
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Zwirner, Johann, Simone Bohnert, Heike Franke, Jack Garland, Niels Hammer, Dustin Möbius, Rexson Tse, and Benjamin Ondruschka. "Assessing Protein Biomarkers to Detect Lethal Acute Traumatic Brain Injuries in Cerebrospinal Fluid." Biomolecules 11, no. 11 (October 25, 2021): 1577. http://dx.doi.org/10.3390/biom11111577.

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Diagnosing traumatic brain injury (TBI) from body fluids in cases where there are no obvious external signs of impact would be useful for emergency physicians and forensic pathologists alike. None of the previous attempts has so far succeeded in establishing a single biomarker to reliably detect TBI with regards to the sensitivity: specificity ratio in a post mortem setting. This study investigated a combination of body fluid biomarkers (obtained post mortem), which may be a step towards increasing the accuracy of biochemical TBI detection. In this study, serum and cerebrospinal fluid (CSF) samples from 30 acute lethal TBI cases and 70 controls without a TBI-related cause of death were evaluated for the following eight TBI-related biomarkers: brain-derived neurotrophic factor (BDNF), ferritin, glial fibrillary acidic protein (GFAP), interleukin 6 (IL-6), lactate dehydrogenase, neutrophil gelatinase-associated lipocalin (NGAL), neuron-specific enolase and S100 calcium-binding protein B. Correlations among the individual TBI biomarkers were assessed, and a specificity-accentuated threshold value analysis was conducted for all biomarkers. Based on these values, a decision tree modelling approach was performed to assess the most accurate biomarker combination to detect acute lethal TBIs. The results showed that 92.45% of acute lethal TBIs were able to be diagnosed using a combination of IL-6 and GFAP in CSF. The probability of detecting an acute lethal TBI was moderately increased by GFAP alone and considerably increased by the remaining biomarkers. BDNF and NGAL were almost perfectly correlated (p = 0.002; R2 = 0.944). This study provides evidence that acute lethal TBIs can be detected to a high degree of statistical accuracy using forensic biochemistry. The high inter-individual correlations of biomarkers may help to estimate the CSF concentration of an unknown biomarker, using extrapolation techniques.
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Savage, William J., Zongming Fu, Emily Barron-Casella, Pratima Dulloor, Jacky Jennings, Elizabeth Dackiw, Kimberly Jones, et al. "Glial Fibrillary Acidic Protein as a Plasma Biomarker of Brain Injury in Children with Sickle Cell Disease." Blood 114, no. 22 (November 20, 2009): 1512. http://dx.doi.org/10.1182/blood.v114.22.1512.1512.

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Abstract Abstract 1512 Poster Board I-535 Introduction In children with sickle cell disease (SCD), silent cerebral infarct (SCI) is an independent risk factor for lower IQ, poorer school performance, and overt stroke. MRI is the only method to identify patients with SCI. A blood biomarker of SCI in patients with sickle cell disease (SCD) would fill a clinical void because blood is easy to obtain and measure, a biomarker may determine risk of or progression of neurologic injury to overt stroke, and a biomarker could benchmark current and new therapies for SCI and other subclinical forms of neurologic injury in SCD. We hypothesized that an unbiased proteomics screen of plasma from sickle cell patients would yield biomarkers of brain injury. Methods A cross-sectional sample of children 5-14 years old with sickle cell disease (HbSS and HbSB0) who were screened for the Silent Infarct Transfusion (SIT) Trial (ClinicalTrials.gov NCT00072761) were studied (n=258) along with 60 age-matched healthy controls and 28 adults with overt brain injury. For biomarker discovery, plasma underwent depletion of hemoglobin with nickel- nitrilotriacetic acid and immunoaffinity depletion of the 12 most abundant plasma proteins. After fractionation by reverse phase liquid chromatography over a C18 column and acetonitrile gradient and trypsin digestion, peptide spectra from each fraction were obtained by LC/MS/MS (LTQ-Orbitrap) and were searched using X!Tandem and human IPI database version 3.5. Post search analysis was performed using Proteomics Analysis Software System (Integrated Analysis Inc., Bethesda, MD). An electrochemiluminescent immunoassay was developed for one of the candidate proteins identified, glial fibrillary acidic protein (GFAP), for protein validation (MesoScale Discovery). Results GFAP, a brain-specific intermediate filament known to be a marker of acute stroke and head trauma in adults, was identified in discovery sample plasma. Four percent of sickle cell subjects in steady-state had plasma GFAP concentrations similar to stroke and brain surgery controls (>0.45 ng/mL). Among sickle cell subjects 5-14 years old screened for the SIT Trial, 9.3% had GFAP concentrations above the 95th percentile of age-matched controls (95th percentile cutoff: 0.227 ng/mL; p=0.08). Sickle cell subjects with silent cerebral infarct (SCI) had more elevations above the normal 95th percentile (10/69; 14.5%) than those without SCI (9/131; 6.8%), although this difference was not statistically significant (p=0.08). The sensitivity of GFAP as a marker of brain injury was demonstrated in a case of an 11 year-old child with HbSS and acute stroke in which plasma GFAP was 1.52 ng/mL (6 times the normal control 95th percentile) before the stroke was clinically evident and peaked at 2.83 ng/mL. We discovered GFAP as a circulating brain protein in plasma of children with SCD. Plasma GFAP is a marker of acute stroke in sickle cell disease but discriminates only minimally between SCI and non-SCI status in the SIT Trial using baseline cross-sectional samples. Four percent of children with sickle disease 5-14 years old have plasma GFAP levels similar to controls with severe brain injury without clinical evidence of overt stroke. Conclusions Elevations in circulating brain proteins such as GFAP show promise as indicators of subacute brain injury in children with SCI, but will require longitudinal studies of plasma GFAP in children with SCI to clarify the utility of GFAP as a plasma biomarker of SCI and a predictor of neurologic risk. Disclosures No relevant conflicts of interest to declare.
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Chaykovskaya, A. D., M. P. Topuzova, A. M. Makhanova, A. G. Mikheeva, D. S. Korotkova, M. L. Pospelova, E. B. Panina, et al. "Role of neuron-specific enolase, glial fibrillar acidic protein and NR2-antibodies in early diagnostic of ischemic stroke." Translational Medicine 8, no. 5 (December 18, 2021): 5–20. http://dx.doi.org/10.18705/2311-4495-2021-8-5-5-20.

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Background. Application of a biomarker panel during the acute period of the ischemic stroke (IS) can contribute to a more accurate and prompter diagnostics and verification of the optimal approach to a patients’ management.Objective. We aimed to clarify values of neuron-specific enolase (NSE), glial fibrillar acidic protein (GFAP) and antibodies for NMDA receptor’s NR2-subunit (NR2-antibodies) in the acute period of IS, to compare with such values in patients without IS, to assess their relationship with severity of neurological deficit and short-term outcome and also to establish sensitivity and specificity of the biomarker panel.Design and methods. 63 patients with IS and 31 people (11 with chronic brain ischemia and 20 healthy individuals) as controls were included. Results. NSE and GFAP values in IS group exceeded reference values at the onset of disease, lowering significally by 10-14 day, while NR2-antibodies’ values were lower at the onset of the disease compared with controls, rising by 10-14 day. In patients with unfavourable short-term outcome higher levels of NSE, GFAP and NR2-antibodies were found. A panel of such biomarkers has higher sensitivity and specificity than each of them individually.Conclusion. Researched substances can be used in a biomarker panel for IS diagnostics, brain damage monitoring, patient’s condition evaluation and short outcome prognosing.
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Ebenau, Jarith L., Wiesje Pelkmans, Inge M. W. Verberk, Sander C. J. Verfaillie, Karlijn A. van den Bosch, Mardou van Leeuwenstijn, Lyduine E. Collij, et al. "Association of CSF, Plasma, and Imaging Markers of Neurodegeneration With Clinical Progression in People With Subjective Cognitive Decline." Neurology 98, no. 13 (February 2, 2022): e1315-e1326. http://dx.doi.org/10.1212/wnl.0000000000200035.

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Background and ObjectivesMultiple biomarkers have been suggested to measure neurodegeneration (N) in the AT(N) framework, leading to inconsistencies between studies. We investigated the association of 5 N biomarkers with clinical progression and cognitive decline in individuals with subjective cognitive decline (SCD).MethodsWe included individuals with SCD from the Amsterdam Dementia Cohort and SCIENCe project, a longitudinal cohort study (follow-up 4±3 years). We used the following N biomarkers: CSF total tau (t-tau), medial temporal atrophy visual rating on MRI, hippocampal volume (HV), serum neurofilament light (NfL), and serum glial fibrillary acidic protein (GFAP). We determined correlations between biomarkers. We assessed associations between N biomarkers and clinical progression to mild cognitive impairment or dementia (Cox regression) and Mini-Mental State Examination (MMSE) over time (linear mixed models). Models included age, sex, CSF β-amyloid (Aβ) (A), and CSF p-tau (T) as covariates, in addition to the N biomarker.ResultWe included 401 individuals (61±9 years, 42% female, MMSE 28 ± 2, vascular comorbidities 8%–19%). N biomarkers were modestly to moderately correlated (range r −0.28 – 0.58). Serum NfL and GFAP correlated most strongly (r 0.58, p < 0.01). T-tau was strongly correlated with p-tau (r 0.89, p < 0.01), although these biomarkers supposedly represent separate biomarker groups. All N biomarkers individually predicted clinical progression, but only HV, NfL, and GFAP added predictive value beyond Aβ and p-tau (hazard ratio 1.52 [95% CI 1.11–2.09]; 1.51 [1.05–2.17]; 1.50 [1.04–2.15]). T-tau, HV, and GFAP individually predicted MMSE slope (range β −0.17 to −0.11, p < 0.05), but only HV remained associated beyond Aβ and p-tau (β −0.13 [SE 0.04]; p < 0.05).DiscussionIn cognitively unimpaired older adults, correlations between different N biomarkers were only moderate, indicating they reflect different aspects of neurodegeneration and should not be used interchangeably. T-tau was strongly associated with p-tau (T), which makes it less desirable to use as a measure for N. HV, NfL, and GFAP predicted clinical progression beyond A and T. Our results do not allow to choose one most suitable biomarker for N, but illustrate the added prognostic value of N beyond A and T.Classification of EvidenceThis study provides Class II evidence that HV, NfL, and GFAP predicted clinical progression beyond A and T in individuals with SCD.
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Dissertations / Theses on the topic "GFAP biomarker"

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Wiegmann, Tim [Verfasser], Hendrik [Gutachter] Milting, and Christos [Gutachter] Krogias. "Nutzen von GFAP und S100B als prädiktiver Biomarker für neurologische Komplikationen bei Patienten mit einem Herzunterstützungssystem / Tim Wiegmann ; Gutachter: Hendrik Milting, Christos Krogias." Bochum : Ruhr-Universität Bochum, 2016. http://d-nb.info/1123283230/34.

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Holler, Alicia Leanne. "Functional 3-D Cellulose and Nitrocellulose Paper-based, Microfluidic Device Utilizing ELISA Technology for the Detection/Distinction Between Hemorrhagic and Ischemic Strokes." DigitalCommons@CalPoly, 2016. https://digitalcommons.calpoly.edu/theses/1707.

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The purpose of this thesis project is to demonstrate and evaluate an enzyme-linked immunosorbent assay (ELISA) on a paper microfluidic device platform. The integration of ELISA technology onto paper microfluidic chips allows for a quantitative detection of stroke biomarkers, such as glial fibrillary acidic protein (GFAP). Dye experiments were performed to confirm fluid connectivity throughout the 3D chips. Several chip and housing designs were fabricated to determine an optimal design for the microfluidic device. Once this design was finalized, development time testing was performed. The results confirmed that the paper microfluidic device could successfully route fluid throughout its channels at a reasonable rate. For the biochemistry portion of this thesis project, antibodies were selected to target the intended stroke biomarker: GFAP. However, due to antibody pairing complications, the protein chosen for this project was natural human cardiac troponin T, which is elevated in the bloodstream of patients who have suffered a stroke. Several antibody experiments were performed to help finalize the procedure for performing an ELISA on the paper chip. The final antibody experiment was able to demonstrate that a paper microfluidic device utilizing ELISA techniques can successfully detect a stroke biomarker at physiologically relevant concentrations. Overall, this project supported the ability to accurately and effectively diagnose stroke in a timely manner through the use of a paper microfluidic device.
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Trautz, Florian. "Überlebenszeitabhängige Änderungen der zerebralen IL-6- und GFAP-Expression nach letalen Schädel-Hirn-Traumen." 2020. https://ul.qucosa.de/id/qucosa%3A73840.

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Die vorliegende Arbeit untersuchte die Verwendbarkeit einer semiquantitativen Auszählung des zellulär sezernierten Zytokins Interleukin-6 (IL-6) und des zerebralen Intermediärfilamentes Saures Gliafaserprotein (GFAP) hinsichtlich ihrer Aussagekraft zur Detektion eines Schädel-Hirn-Traumas (SHT) und der Abschätzung des Überlebenszeitintervalls zwischen Erleiden der Gewalteinwirkung und dem Todeseintritt. Hierzu wurden Hirngewebsproben von 75 Verstorbenen im Rahmen gerichtlich angeordneter Obduktionen verwendet: 54 Fälle wiesen ein zum Tode führendes Schädel-Hirn-Trauma auf (Fallgruppe) und 21 Fälle mit kardiovaskulär bedingtem Todeseintritt wurden als Kontrollgruppe untersucht. Das maximale postmortale Intervall betrug 6 Tage. Gewebsproben definierter Hirnareale (Kortex, Perikontusionszone (PKZ), Hippocampus, Kleinhirn) wurden mit IL-6- und GFAP-Antikörpern immunhistochemisch untersucht und die positiv gefärbten Zellen semiquantitativ erfasst. Die Ergebnisse wurden zu den Überlebenszeiten nach Trauma korreliert und mit der Kontrollgruppe verglichen. Es zeigte sich für IL-6 und GFAP ein statistisch signifikanter Konzentrationsanstieg mit zunehmender Überlebenszeit in der PKZ und in Hypoxie-sensiblen Arealen des Zentralen Nervensystems (ZNS). Die Methode war geeignet, SHT-Fälle von den Kontrollen bei Überschreiten ermittelter Schwellenwerte in Bezug auf die Färbungen zu differenzieren. Die präsentierten Ergebnisse belegen den potentiellen Nutzen der beiden gewählten immunhistochemischen Marker als Ergänzung zur gängigen SHT-Wundalterdiagnostik in der forensischen Praxis.
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Rawji, Khalil S. "A Comparative Analysis of the Neurochemical Properties of Olfactory Ensheathing Cells and their Biocompatibility in Various Biomatrices." Thesis, 2012. http://hdl.handle.net/1974/7335.

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Olfactory ensheathing cells (OECs) are the chief glial population of the mammalian olfactory nervous system and are thought to be responsible for the successful directional growth of new olfactory axons throughout the life of adult mammals. Due to this unique property, OECs have been targeted as a potential cellular transplantation therapy for spinal cord injury. In order to effectively isolate OECs for intraspinal transplantation, more knowledge must be gained on their phenotypic properties. We investigated the neurochemical features of OECs in a variety of mammalian species (including hamsters, rabbits, monkeys, mice, and pigs) using three biomarkers: glial fibrillary acidic protein (GFAP), S100β, and α-smooth muscle actin (αSMA). In addition, we tested the ability of a few biomatrices to sustain and promote OEC growth and survival in vitro. The rationale for using biomatrices is to provide a supportive environment for glial and axonal growth in the spinal lesion. Here, we found that mucosal and bulbar OECs from all five of the aforementioned mammalian species express S100β. Expression of GFAP, however, was not consistent across the five species. Both mucosal and bulbar OECs of monkeys express αSMA; only bulbar OECs of hamsters and only mucosal OECs of rabbits express αSMA as well. Though αSMA immunostaining was not detected in the OECs of adult mice, in adult mutant mice lacking αSMA expression, OECs displayed perturbed ultrastructural morphology. None of the biomatrices used (methacrylated glycol chitosan, arginine-glycine-aspartic acid – grafted methacrylated glycol chitosan, and agarose) were able to promote OEC proliferation. Isolated strips of rodent olfactory lamina propria (the deep connective tissue layer in the olfactory mucosa containing primary sensory axons and OECs) showed sustained growth when cultured for 10 days. In sum, these findings highlight the following points: the efficacy of S100β and αSMA as biomarkers for mammalian OECs in vivo; the potential for isolated strips of lamina propria to provide a natural, supportive environment for OECs during intraspinal transplantation; the failure of methacrylated glycol chitosan and its derivatives, as well as agarose, to promote OEC proliferation.
Thesis (Master, Neuroscience Studies) -- Queen's University, 2012-07-27 15:29:47.642
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Chang, Shiou-Ming, and 張修明. "Characterization of the activation of a GFP expression system driven by p21Cip1/Waf1promoter as a biomarker of cellular senescence in mammalian cells." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/03292468454478382947.

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碩士
國立屏東科技大學
生物科技研究所
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Advances in medicine and public health resulted in a large increase in the average life span of humans, whereas aging of the population is also getting more and more obvious. Therefore, how to maintain a healthy, quality life in the old age of an individual has become an important issue. The purpose of this study is to establish a cell-based screening system which not only can be applied to the screening of anti-aging reagents from large amounts of samples, but also can be a tool for the study of molecular mechanism of cellular senescence. However, the prerequisite for the efficiency of this system is to develop a method that can readily detect the aging of cell in vivo.Cellular senescence was defined as the irreversible arrest of cells in the G1 phase of cell cycle. Study of the molecular mechanism of cellular senescence showed that p21cip1/waf1 is highly expressed in aged cells. p21cip1/waf1 was demonstrated to induce the arrest of cell cycle in G1 phase, resulting in entry of cell into the senescence state. In this project, various lengths of DNA fragments were subcloned from the p21cip1/waf1 promoter region of human genomic DNA, and ligated into the upstream of the gene of green fluorescent protein (GFP) in an expression vector. The vector was then stably transfected into BHK-21 cells, a baby hamster kidney normal cell line. The expression level of GFP was then be analyzed by fluorescent microscope and flow cytometer. The data demonstrated that induction of the aging of transfected BHK-21 cell was accompanied by the elevated expression of GFP. In addition, whether different regions of the p21cip1/waf1 promoter play important roles in the process of cellular aging was characterized as well.
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Book chapters on the topic "GFAP biomarker"

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Abdi, Fahmida, Ann M. Simpson, Sara Lal, and Kaneez Fatima Shad. "Early Predictive Biomarkers for Hypertension Using Human Fetal Astrocytes." In Erythrocyte - A Peripheral Biomarker For Infection and Inflammation. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98561.

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Hypertension is a major risk factor for cardiovascular and cerebrovascular diseases, causing high numbers of deaths and /or disabilities worldwide. Previous studies have reported numerous biomolecules, such as, triglycerides and fibrinogen as biomarkers of hypertension (HTN), but none of these biomolecules could be considered as ‘true’ predictive biomarkers as they were produced after the establishment of HTN. Therefore, there is an urgent need for identifying and monitoring molecules that are linked to early pre-HTN stages, that is, prior to the onset of HTN. Astrocytes are the most abundant cells in the nervous system and through their long processes, astrocytes can communicate with both neuronal and non-neuronal cells such as endothelial cells lining blood vessels. Thus, any biochemical changes in astrocytes will affect both blood vessels and neurons. We are using human fetal astrocytes (HFAs) to investigate the molecules which may possibly act as early predictive biomarkers for hypertension. Astrocytic processes are mostly supported by the intermediate filaments, an example is the glial fibrillary acidic protein (GFAP) which is a type III intermediate filament. Elevated GFAP levels are being considered as a marker of astroglial injury, indicating the conversion of non-reactive (A2) into reactive (A1) astrocytes. Our initial immunohistochemistry studies using anti-GFAP antibodies on astrocytes from spontaneous hypertensive rats (SHRs) and their normal counter parts (WKY) rats showed a similar profile to that of reactive (A1) and non-reactive (A2) HFAs, respectively. Numerous studies point to a significant role of calcium ion channel proteins in hypertension, and calcium channel blockers such as Amlodipine (Norvasc) Diltiazem (Cardizem) are commonly used as antihypertensive drugs. By using liquid chromatography–tandem mass spectrometry (LC–MS/MS) we observed that reactive (A1) astrocytes, contain more calcium-activated proteins such as calpain, calpastatin, cathepsin and mitogen activated protein kinase (MAPK) as compare to normal (A2) HFAs, suggesting their possible link to the future onset of HTN. Hence these proteins could be considered as potential early predictive biomarkers of HTN.
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Papa, Linda. "Acute Assessment of Mild Traumatic Brain Injury." In Neurotrauma, edited by John K. Yue, Ethan A. Winkler, Hansen Deng, Amy J. Markowitz, Kevin K. W. Wang, and Geoffrey T. Manley, 101–10. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190279431.003.0009.

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Most patients with mild TBI (mTBI) are discharged from the emergency department (ED) after a normal clinical examination and a reasonable period of observation and/or following a negative head computed tomography (CT) scan. Studies indicate that about 30% of mTBI patients discharged from the ED will have symptoms at 3 months and up to 15% will be symptomatic at 1 year post-injury. Serum markers have the potential to better manage patients with mTBI. Unlike clinical variables, serum biomarkers offer a more objective measure of injury and could complement clinical decision-making. In 2018, the US Food and Drug Administration approved the use of a blood test combining UCH-L1 and GFAP for detecting lesions on CT scan in adults with mTBI within 12 hours of injury. Introducing biomarkers into clinical practice requires well-designed studies with adequate sample sizes, proper sample timing, stringent reporting of outcome measures, and well-described assay performance characteristics.
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"), confocal laser scanning microscopy (Eberl et al. 1997) or enumerated by flow cytometry (Tombolini et al. 1997). A further advantage of GFP, over other biomarkers, is the fact that no other energy source or substrate addition is required, other than oxygen during initial formation of the chromophore. Therefore, the GFP biomarker holds tremendous promise for elucidation of specific bacterial numbers and their behaviour, colonization, distribution, interaction, and movement in situ in a diversity of environmental sample types. Additionally, mutations have been introduced into the GFP gene in order to produce fluorescence signals with altered properties (Heim et al. 1994, Delagrave et al. 1995, Crameri et 1996, Heim and Tsien 1996). For example, one of the mutants (P4) is a." In Recent Advances in Marine Biotechnology, Vol. 8, 237. CRC Press, 2003. http://dx.doi.org/10.1201/9781482279986-29.

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"or phenotype to enable monitoring in a given environment (Jansson and De Bruijn 1999). These biomarkers therefore fill a surrogate role, supplying an assayable gene product when an assay for a gene product of interest is not available or is very difficult to perform. Two biomarkers which have become extremely attractive for monitoring microbial communities and activity are the genes encoding luciferase enzymes and the green fluorescent protein (GFP). This is mainly due to their ease of use, along with the ability to perform the assays in a nondestructive manner. Such non­ destructive assays allow for repeated experiments to be performed on the same sample, and so changes of a microbial community can be observed." In Recent Advances in Marine Biotechnology, Vol. 8, 234–35. CRC Press, 2003. http://dx.doi.org/10.1201/9781482279986-27.

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Conference papers on the topic "GFAP biomarker"

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Ciesielski, Michael J., Phillip Galbo, Sheila Figel, Laura Wiltsie, Cheryl Frank, Jingxin Qiu, and Robert A. Fenstermaker. "Abstract 2725: Circulating CD9-GFAP-survivin exosomes during active specific immunotherapy, a potential biomarker for glioma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2725.

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Rocha, Andreia, Bruna Bellaver, Luiza Machado, Carolina Soares, Pâmela C. L. Ferreira, Samuel Greggio Gianina T. Venturin, Jaderson C. da Costa, Diogo O. Souza, and Eduardo R. Zimmer. "TEMPORAL CHANGES IN ASTROCYTES ON A TRANSGENIC RAT MODEL OF AD." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda023.

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Background: Recent evidences have pointed to astrocytes as important players in the Alzheimer’s Disease (AD) pathogenesis. Objective: With this in mind, we aim to longitudinally investigate astrocyte changes in a new important AD transgenic model, the TgF344-AD rat, the first animal model harboring human APP/PS1 mutations which presents age-dependent amyloid and tau pathology. Methods: TgF344-AD rats and wild type littermates were evaluated in three time points: 3, 6 and 9 months of age. Rats underwent a [18F]FDG-microPET, a spatial-memory, an astrocytes CSF biomarkers (ELISA multiplex) and a glutamate uptake (ex-vivo slices) analysis. Examination of further time-points are being conducted at the moment. Results: At 9 months of age, TgF344-AD animals presented an increase in the cortical [18F]FDG uptake and a decline in their alternance performance in the Y-maze task. In the CSF analysis, GFAP was elevated at both 6 months and 9 months, while S100B presented a decrease at 6mo. Additionally, the cortical glutamate uptake was increased at 9 months. Conclusion: This study is the first to longitudinally investigate the in vivo brain glucose metabolism in the TgF344-AD rat model. Our results suggest that this model presents an early increase on glucose metabolism which may be related to astrocytes activation and the increase of glutamate uptake by these cells. Furthermore, we also identified a spatial memory impairment at the same age.
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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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