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Academic literature on the topic 'Myelin Content'

Author: Grafiati

Published: 26 April 2025

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Journal articles on the topic "Myelin Content"

Kim, Joo-won, Thomas P. Naidich, Benjamin A. Ely, Essa Yacoub, Federico De Martino, Mary E. Fowkes, Wayne K. Goodman, and Junqian Xu. "Human habenula segmentation using myelin content." NeuroImage 130 (April 2016): 145–56. http://dx.doi.org/10.1016/j.neuroimage.2016.01.048.

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Weickenmeier, J., R. de Rooij, S. Budday, P. Steinmann, T. C. Ovaert, and E. Kuhl. "Brain stiffness increases with myelin content." Acta Biomaterialia 42 (September 2016): 265–72. http://dx.doi.org/10.1016/j.actbio.2016.07.040.

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Bouhrara, Mustapha, Joseph S. R. Alisch, Nikkita Khattar, Richard W. Kim, Abinand C. Rejimon, Luis E. Cortina, Wenshu Qian, Luigi Ferrucci, Susan M. Resnick, and Richard G. Spencer. "Association of cerebral blood flow with myelin content in cognitively unimpaired adults." BMJ Neurology Open 2, no. 1 (July 2020): e000053. http://dx.doi.org/10.1136/bmjno-2020-000053.

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BackgroundMyelin loss and cerebral blood flow (CBF) decline are central features of several neurodegenerative diseases. Myelin maintenance through oligodendrocyte metabolism is an energy-demanding process, so that myelin homeostasis is particularly sensitive to hypoxia, hypoperfusion or ischaemia. However, in spite of its central importance, little is known about the association between blood supply and myelin integrity.ObjectiveTo assess associations between cortical and subcortical CBF, and subcortical myelin content, in critical brain white matter regions.Materials and methodsMRI was performed on a cohort of 67 cognitively unimpaired adults. Using advanced MRI methodology, we measured whole-brain longitudinal and transverse relaxation rates (R1 and R2), sensitive but non-specific markers of myelin content, and myelin water fraction (MWF), a direct surrogate of myelin content, as well as regional CBF, from each of these participants.ResultsAll quantitative relaxometry metrics were positively associated with CBF in all brain regions evaluated. These associations between MWF or R1 and CBF, and, to a lesser extent, between R2 and CBF, were statistically significant in most brain regions examined, indicating that lower regional cortical or subcortical CBF corresponds to a decrease in local subcortical myelin content. Finally, all relaxometry metrics exhibited a quadratic, inverted U-shaped, association with age; this is attributed to the development of myelination from young to middle age, followed by progressive loss of myelin in later years.ConclusionsIn this first study examining the association between local blood supply and myelin integrity, we found that myelin content declines with CBF across a wide age range of cognitively normal subjects.

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Laporte, John P., Mary E. Faulkner, Zhaoyuan Gong, Mohammad A. B. S. Akhonda, Luigi Ferrucci, Josephine M. Egan, and Mustapha Bouhrara. "Hypertensive Adults Exhibit Lower Myelin Content: A Multicomponent Relaxometry and Diffusion Magnetic Resonance Imaging Study." Hypertension 80, no. 8 (August 2023): 1728–38. http://dx.doi.org/10.1161/hypertensionaha.123.21012.

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BACKGROUND: It is unknown whether hypertension plays any role in cerebral myelination. To fill this knowledge gap, we studied 90 cognitively unimpaired adults, age range 40 to 94 years, who are participants in the Baltimore Longitudinal Study of Aging and the Genetic and Epigenetic Signatures of Translational Aging Laboratory Testing to look for potential associations between hypertension and cerebral myelin content across 14 white matter brain regions. METHODS: Myelin content was probed using our advanced multicomponent magnetic resonance relaxometry method of myelin water fraction, a direct and specific magnetic resonance imaging measure of myelin content, and longitudinal and transverse relaxation rates ( R 1 and R 2 ), 2 highly sensitive magnetic resonance imaging metrics of myelin content. We also applied diffusion tensor imaging magnetic resonance imaging to measure fractional anisotropy, mean diffusivity, radial diffusivity, and axial diffusivity values, which are metrics of cerebral microstructural tissue integrity, to provide context with previous magnetic resonance imaging findings. RESULTS: After adjustment of age, sex, systolic blood pressure, smoking status, diabetes status, and cholesterol level, our results indicated that participants with hypertension exhibited lower myelin water fraction, fractional anisotropy, R 1 and R 2 values and higher mean diffusivity, radial diffusivity, and axial diffusivity values, indicating lower myelin content and higher impairment to the brain microstructure. These associations were significant across several white matter regions, particularly in the corpus callosum, fronto-occipital fasciculus, temporal lobes, internal capsules, and corona radiata. CONCLUSIONS: These original findings suggest a direct association between myelin content and hypertension and form the basis for further investigations including longitudinal assessments of this relationship.

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Kozko, Volodymyr, Maryna Hvozdetska-Shaar, Anton Sokhan, Kateryna Yurko, and Ganna Solomennyk. "Myelin basic protein and its diagnostic value in HIV-infected individuals with 4th clinical stage and neuroinfections." ScienceRise: Medical Science, no. 2(41) (April 5, 2021): 28–32. http://dx.doi.org/10.15587/2519-4798.2021.228189.

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It was shown that in HIV-infected patients, pathomorphological changes in the white matter in the form of demyelinization are already observed in the early stages of the disease. The most studied marker of this process is myelin basic protein that can be detected in cerebrospinal fluid or serum immediately after acute myelin breakdown. The aim. To assess the diagnostic value of myelin basic protein content in serum and cerebrospinal fluid of HIV-infected individuals with 4th clinical stage and central nervous system opportunistic infections. Materials and methods. Using ELISA with diagnostic kit “MBP ELISA” (Ansh Labs, USA), we studied the myelin basic protein content in serum and cerebrospinal fluid of 53 HIV-infected patients with 4th clinical stage and central nervous system opportunistic infections depending on its etiology, the outcome of the diseases and according to Glasgow coma scale score. As well correlation analysis with some laboratory and clinical indicators was performed. Results. We found significantly increased myelin basic protein content in both cerebrospinal fluid and serum of HIV-infected patients 4th clinical stage with central nervous system opportunistic infections compared to control (p˂0.01), which indicate the presence of active demyelinization in central nervous system. The highest cerebrospinal fluid myelin basic protein was registered in patients with an unfavourable outcome of the disease, as death or residual neurologic deficit, and patients with cerebral toxoplasmosis. The cerebrospinal fluid myelin basic protein had an association with the size of white matter lesions on magnetic resonance imaging and serum myelin basic protein content. Conclusions. Myelin basic protein detection in cerebrospinal fluid as well as in serum can serve as an additional quantitative marker of myelin disruption, which can be used along with magnetic resonance imaging for the diagnosis improvement and prognosis of central nervous system opportunistic infections in HIV-infected individuals with 4th clinical stage

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Träger, Jennica, Katharina Widder, Andreas Kerth, George Harauz, and Dariush Hinderberger. "Effect of Cholesterol and Myelin Basic Protein (MBP) Content on Lipid Monolayers Mimicking the Cytoplasmic Membrane of Myelin." Cells 9, no. 3 (February 25, 2020): 529. http://dx.doi.org/10.3390/cells9030529.

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Myelin basic protein (MBP) is located in the insulating covers of nerve cells in the brain and spinal cord. By interacting with lipid membranes, it is responsible for compaction of the myelin sheath in the central nervous system, which is weakened in demyelinating diseases. The lipid composition of the myelin leaflet has a high impact on the interaction between the membrane and MBP. Cholesterol is present in the cytoplasmic leaflet with a rather high amount of 44% (mol%). In this study, the focus is on the effect of cholesterol, mainly by varying its content, on the interaction of MBP with a lipid monolayer. Therefore, Langmuir lipid monolayers mimicking the cytoplasmic membrane of myelin and monolayers with variations of cholesterol content between 0% and 100% were measured at the air/water interface with additional imaging by fluorescence microscopy. All experiments were performed with and without bovine MBP to study the dependence of the interaction of the protein with the monolayers on the cholesterol content. The native amount of 44% cholesterol in the monolayer combines optima in the order of the monolayer (presumably correlating to compaction and thermodynamic stability) and protein interaction and shows unique features in comparison to lower or higher cholesterol contents.

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Qiu, Yidan, Shenglin She, Shufei Zhang, Fengchun Wu, Qunjun Liang, Yongjun Peng, Haishan Yuan, Yuping Ning, Huawang Wu, and Ruiwang Huang. "Cortical myelin content mediates differences in affective temperaments." Journal of Affective Disorders 282 (March 2021): 1263–71. http://dx.doi.org/10.1016/j.jad.2021.01.038.

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Dao, Elizabeth, Roger Tam, Ging-Yuek R. Hsiung, Lisanne ten Brinke, Rachel Crockett, Cindy K. Barha, Youngjin Yoo, et al. "Exploring the Contribution of Myelin Content in Normal Appearing White Matter to Cognitive Outcomes in Cerebral Small Vessel Disease." Journal of Alzheimer's Disease 80, no. 1 (March 9, 2021): 91–101. http://dx.doi.org/10.3233/jad-201134.

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Background: Myelin damage is a salient feature in cerebral small vessel disease (cSVD). Of note, myelin damage extends into the normal appearing white matter (NAWM). Currently, the specific role of myelin content in cognition is poorly understood. Objective: The objective of this exploratory study was to investigate the association between NAWM myelin and cognitive function in older adults with cSVD. Methods: This exploratory study included 55 participants with cSVD. NAWM myelin was measured using myelin water imaging and was quantified as myelin water fraction (MWF). Assessment of cognitive function included processing speed (Trail Making Test Part A), set shifting (Trail Making Test Part B minus A), working memory (Verbal Digit Span Backwards Test), and inhibition (Stroop Test). Multiple linear regression analyses assessed the contribution of NAWM MWF on cognitive outcomes controlling for age, education, and total white matter hyperintensity volume. The overall alpha was set at ≤0.05. Results: After accounting for age, education, and total white matter hyperintensity volume, lower NAWM MWF was significantly associated with slower processing speed (β = –0.29, p = 0.037) and poorer working memory (β= 0.30, p = 0.048). NAWM MWF was not significantly associated with set shifting or inhibitory control (p > 0.132). Conclusion: Myelin loss in NAWM may play a role in the evolution of impaired processing speed and working memory in people with cSVD. Future studies, with a longitudinal design and larger sample sizes, are needed to fully elucidate the role of myelin as a potential biomarker for cognitive function.

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Huynh, Thao N., Matthew C. Havrda, George J. Zanazzi, Catherine C. Y. Chang, and Ta Yuan Chang. "Inhibiting the Cholesterol Storage Enzyme ACAT1/SOAT1 in Myelin Debris-Treated Microglial Cell Lines Activates the Gene Expression of Cholesterol Efflux Transporter ABCA1." Biomolecules 14, no. 10 (October 14, 2024): 1301. http://dx.doi.org/10.3390/biom14101301.

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Aging is the major risk factor for Alzheimer’s disease (AD). In the aged brain, myelin debris accumulates and is cleared by microglia. Phagocytosed myelin debris increases neutral lipid droplet content in microglia. Neutral lipids include cholesteryl esters (CE) and triacylglycerol (TAG). To examine the effects of myelin debris on neutral lipid content in microglia, we added myelin debris to human HMC3 and mouse N9 cells. The results obtained when using 3H-oleate as a precursor in intact cells reveal that myelin debris significantly increases the biosynthesis of CE but not TAG. Mass analyses have shown that myelin debris increases both CE and TAG. The increase in CE biosynthesis was abolished using inhibitors of the cholesterol storage enzyme acyl-CoA:cholesterol acyltransferase 1 (ACAT1/SOAT1). ACAT1 inhibitors are promising drug candidates for AD treatment. In myelin debris-loaded microglia, treatment with two different ACAT1 inhibitors, K604 and F12511, increased the mRNA and protein content of ATP-binding cassette subfamily A1 (ABCA1), a protein that is located at the plasma membrane and which controls cellular cholesterol disposal. The effect of the ACAT1 inhibitor on ABCA1 was abolished by preincubating cells with the liver X receptor (LXR) antagonist GSK2033. We conclude that ACAT1 inhibitors prevent the accumulation of cholesterol and CE in myelin debris-treated microglia by activating ABCA1 gene expression via the LXR pathway.

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Walker, Keenan. "COMBINED USE OF NOVEL MR IMAGING AND FLUID BIOMARKERS REVEAL DETERMINANTS OF MYELIN AND AXONAL LOSS WITH AGING." Innovation in Aging 7, Supplement_1 (December 1, 2023): 386. http://dx.doi.org/10.1093/geroni/igad104.1279.

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Abstract Cerebral white matter damage is a feature of Alzheimer’s disease, vascular dementia, and other neurodegenerative conditions, yet little is known about the molecular underpinnings of key features of white matter pathology. In a series of studies we have used targeted assays and large-scale proteomics platforms to determine how biomarkers of Alzheimer’s disease pathology (Aß42/40 ratio; pTau181), neuronal injury (NfL), reactive astrogliosis (GFAP), and other disease processes relate to state-of-the-art diffusion-based MRI measures of brain myelin content and axonal density in cognitively unimpaired older adults. Using data from the Baltimore Longitudinal Study of Aging (BLSA) and the GESTALT study, we measured plasma biomarkers using the Quanterix Simoa assay (targeted measurement of 4 proteins) and the SomaScan proteomic platform (untargeted measurement of 7000 proteins). Additionally, participants underwent 3T MRI, from which measure of myelin content (defined by myelin water fraction [MWF]) and axonal density (defined by neurite density index [NDI]) were derived. We found an association between higher plasma GFAP and lower myelin content in temporal brain regions. Additionally, higher levels of NfL and GFAP were associated with lower total brain axonal density. Using untargeted proteomics, we identified a set of 155 plasma proteins that were associations with myelin content (P <0.05). Using these findings, we applied machine learning to construct a plasma protein-based predictor of brain myelin content, which we plan to validate in a cohort of individuals with multiple sclerosis: a condition characterized by demyelination.

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Dissertations / Theses on the topic "Myelin Content"

Battiston, Marco. "Quantitative MRI for measuring myelin content in human spinal cord." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10046127/.

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The aim of this thesis is to progress the state-of-the art of quantitative Magnetic Resonance Imaging (MRI) in the human spinal cord, with particular focus on methods sensitive to myelin content. Myelin is a fundamental structure of the central nervous system, ensuring the correct transmission of action potentials along neuronal axons, affected in a number of neurological disorders, first and foremost Multiple Sclerosis (MS). MRI methods to assess myelin in the spinal cord have found limited development, despite the primary involvement of the spinal cord in demyelinating diseases, such as MS where the characterization of spinal cord pathology is key for a better diagnosis, understanding of pathological processes, and evaluation of neuroprotective and reparative treatments. In this thesis, we develop novel methods for the spinal cord to measure parameters that are known to correlate with myelin content, namely the longitudinal relaxation time (T1) and quantitative Magnetization Transfer (qMT) parameters, and we compare them with a large set of myelin sensitive MRI indices in the post mortem MS spinal cord. The thesis is structured as follows: chapter 1 states the problem this thesis attempts to address and provides background information regarding the involvement of the spinal cord in MS; chapter 2 reviews the basic principles of MRI and introduces the theory behind the measurement of surrogate indices of myelin content with MRI; chapter 3 reviews an existing imaging sequence for the spinal cord, extends its use for measuring myelin sensitive parameters and discusses potential improvements for in vivo applications; chapter 4 and chapter 5 propose novel efficient methods to measure T1 and qMT parameters in vivo in the spinal cord; and chapter 6 evaluates the performance of the methods developed in the previous chapter, together with other prospective myelin mapping methods, in the healthy and MS post mortem human spinal cord.

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TURATI, LAURA. "Quantitative Magnetization Transfer imaging for in vivo analysis of myelin content in experimental model of demyelination." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/55300.

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La demielinizzazione è un processo patologico in cui le guaine mieliniche, che rivestono gli assoni, sono danneggiate. La demielinizzazione del sistema nervoso centrale (SNC) è la conseguenza di un insulto diretto o indiretto agli oligodendrociti, cellule del SNC deputate alla produzione ed al mantenimento delle guaine mieliniche. La remielinizzazione è invece l’evento naturale che dovrebbe ripristinare la conduzione dell’impulso elettrico assonale e risolvere i deficit funzionali. Nella sclerosi multipla (SM) la perdita di mielina, in particolare in prossimità delle regioni internodali, è associata al blocco della conduzione nervosa e non è compensata da adeguata remielinizzazione. Lo sviluppo di terapie in grado di controllare il processo di demielinizzazione e la valutazione della loro efficacia è in parte complicato dalla difficoltà di valutare in modo non invasivo lo stato della mielina. Nel presente studio, la tecnica ‘quantitative magnetization transfer-MRI’ (qMT-MRI) è stata utilizzata per valutare il grado di de/remielinizzazione nel modello murino sperimentale indotto da cuprizone, un agente chelante del rame a cui gli oligodendrociti sono particolarmente sensibili. L’ipotesi di base dello studio è che il valore di ‘macromolecular pool size ratio’ (F) sia una stima accurata della densità mielinica in vivo; la correlazione tra analisi in MRI ed istologia è stata finora confermata prevalentemente su campioni di SNC ex vivo. Le corrispondenze tra il parametro F, che risulta dall’interpolazione di differenti misure qMT-MRI, con l’intensità di colorazione per fibre mieliniche (mediante Black Gold II), e con l’intensità di immunofluorescenza per la proteina basica della mielina e per la proteina citoscheletrica neuronale beta-tubulina sono state valutate a differenti time-points, in uno studio sperimentale longitudinale. Topi C57BL/6 e SJL/J sono stati trattati con cuprizone al fine di causare perdita selettiva della mielina, che è seguita da spontanea remielinizzazione dopo la sospensione del trattamento. I risultati hanno confermato una correlazione statisticamente significativa delle misure di F con il contenuto di mielina, e dimostrano l’applicabilità di analisi MRI in vivo nei modelli sperimentali di SM, come strumento per il monitoraggio dello stato della mielina.
Demyelination is a pathological process in which myelin sheaths, around axons, are damaged. Demyelination of the central nervous system (CNS) is the consequence of a direct or indirect insult to oligodendrocytes, specific cells in the CNS that produce and sustain the myelin sheaths. Instead, remyelination is a spontaneous event in which myelin sheaths are restored in demyelinated nerve regions, thus recovering saltatory signal conduction and resolving functional deficits. In multiple sclerosis (MS), the loss of myelin particularly in internode regions is associated with block of nerve conduction and it is not compensated by adequate remyelination. The development of therapies able to control the process of demyelination and the evaluation of their effectiveness is partially complicated by the difficulty in assessing myelin status non-invasively. In the present study, 'quantitative magnetization transfer MRI' (qMT-MRI) technique is used to assess the degree of de/remyelination in an experimental murine model induced by cuprizone, a copper chelator to which oligodendrocytes are preferentially susceptible. The basic hypothesis of the study is that the in vivo measurement of ‘macromolecular pool size ratio’ (F) could be an accurate estimation of myelin density; the correlation between MRI and histology analysis has so far been confirmed mainly on ex vivo CNS samples. The correspondences between the parameter F, which is interpolated from qMT-MRI measures, with the intensity of staining for myelinated fibers (using Black Gold II), and with the intensity of myelin basic protein and neuronal cytoscheletric protein beta-tubulin immunofluorescences were evaluated at different time-points, in an experimental longitudinal study. C57BL/6 and SJL/J mice were fed with cuprizone in order to cause selective myelin loss, which is followed by spontaneous remyelination upon treatment suspension. The results confirmed a statistically significant correlation between F measures and myelin content, and demonstrated the in vivo applicability of MRI analysis to experimental models of MS, as a tool for monitoring myelin status.

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Johnstone, Andrea. "Overcoming Glial-Derived Inhibition of Regeneration in CNS Neurons: From Novel Compounds to Novel Uses for FDA-Approved Compounds." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/631.

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Trauma to the central nervous system (CNS) results in an irreversible disruption of axon tracts, often leading to lifelong functional deficits. Despite a large body of research into the mechanisms that underlie the lack of axonal regeneration after CNS injury, there are currently no effective treatments. One major obstacle involves the presence at injury sites of CNS growth-inhibitory molecules, such as myelin proteins and astrocyte-derived chondroitin sulfate proteoglycans (CSPGs), which act as environmental barriers to axonal regeneration. Our lab recently described the identification and characterization of a novel compound, F05, which promotes growth on inhibitory substrates in vitro. I show that F05 improves regeneration in vivo after acute sensory axon transection as well as after optic nerve crush injury. F05 does not target known signaling molecules involved in CSPG or myelin mediated inhibition but does affect growth cone microtubule dynamics, suggesting a potentially novel mechanism of growth promotion. Using a protein microarray, I show that apoptotic signaling pathways may underlie glial-derived inhibition and its relief by F05. In addition, I employed a comparative gene microarray to show that F05 induces similar changes in gene expression as antipsychotics of the piperazine phenothiazine structural class (PhAPs). Indeed, PhAPs share F05’s ability to overcome glial-derived inhibition of cultured CNS neurons and do so through a mechanism dependent on antagonism of calmodulin. These studies have led to the identification of potentially novel clinical treatments for CNS injury as well as a better understanding of environmentally derived growth-inhibitory signaling mechanisms.

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Yazdan, Panah Arya. "Integrating imaging biomarkers and genetic data to explore the pathophysiology of multiple sclerosis." Electronic Thesis or Diss., Sorbonne université, 2025. http://www.theses.fr/2025SORUS030.

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La sclérose en plaques (SEP) est une maladie chronique, inflammatoire et neurodégénérative du système nerveux central, caractérisée par une démyélinisation et des lésions des voies neuronales dans le cerveau et la moelle épinière. Bien que des avancées significatives aient été réalisées dans le traitement de la composante auto-immune de la SEP, l'approche de sa composante neurodégénérative reste un défi majeur. Cette thèse vise à développer de nouveaux biomarqueurs pour explorer la physiopathologie de la SEP, dans le but de mieux comprendre les mécanismes de la maladie et de soutenir le développement de stratégies thérapeutiques. Pour atteindre cet objectif, trois biomarqueurs clés sont étudiés : (1) le contenu en myéline et (2) le débit sanguin cérébral (DSC), tous deux mesurés par tomographie par émission de positons (TEP), et (3) le volume des plexus choroïdes (PC), un marqueur potentiel de neuroinflammation, quantifié par IRM. L'imagerie TEP permet une quantification précise de la myéline et du DSC dans la matière blanche, en surmontant les limites de l'IRM conventionnelle pour prédire la progression du handicap. Une étude de reproductibilité en test-retest a été réalisée avec un traceur dynamique [11C]PiB TEP pour évaluer la reproductibilité de ces mesures, dans le but d'identifier des biomarqueurs fiables pouvant être appliqués cliniquement. Le deuxième axe de cette thèse explore des techniques d'apprentissage profond pour segmenter automatiquement et contrôler la qualité des mesures de volume des PC en IRM pondérée en T1. Les PC, impliqués dans les processus neuroinflammatoires, constituent un biomarqueur prometteur pour la SEP à différents stades de la maladie. En créant un cadre de segmentation robuste et reproductible, ce travail améliore notre capacité à quantifier les changements de volume des PC avec précision, fournissant des indications sur l'inflammation associée à la progression de la SEP. Enfin, l'architecture génétique du volume des PC est étudiée, en se concentrant sur l'héritabilité de ce phénotype et l'identification des loci génomiques qui pourraient y être associés. À l'aide d'études d'association pangénomique (GWAS) sur des phénotypes dérivés de l'IRM provenant de la UK Biobank, cette recherche identifie plusieurs loci significatifs liés au volume des PC. Des techniques avancées de cartographie génétique, des scores de risque polygénique et la régression de score de liaison ont été employées pour évaluer la corrélation génétique entre le volume des PC et d'autres traits, offrant une vision complète des facteurs génétiques influençant la variabilité des PC. En conclusion, cette thèse représente une approche intégrative pour le développement de biomarqueurs d'imagerie et génomiques afin d'explorer la physiopathologie de la SEP. En combinant TEP et IRM avec des analyses génétiques avancées, elle fournit une perspective multidimensionnelle sur la SEP, identifiant les mécanismes potentiels sous-jacents à la neurodégénérescence et à la neuroinflammation. Ce cadre intégratif soutient le développement de biomarqueurs ciblés susceptibles d'améliorer le diagnostic, le suivi et les interventions thérapeutiques
Multiple sclerosis (MS) is a chronic, inflammatory, and neurodegenerative disease of the central nervous system, marked by demyelination and damage to neural pathways in the brain and spinal cord. While significant advancements have been made in treating the autoimmune aspect of MS, addressing the neurodegenerative component remains a critical challenge. This thesis focuses on developing new biomarkers to explore the pathophysiology of MS, aiming to deepen our understanding of disease mechanisms and support the development of therapeutic strategies. To achieve this, we investigate three key biomarkers: (1) myelin content and (2) cerebral blood flow (CBF), both assessed using positron emission tomography (PET), and (3) choroid plexus (CP) volume, a potential proxy for neuroinflammation, quantified through MRI. PET imaging allows precise quantification of myelin and CBF in the white matter, overcoming the limitations of conventional MRI in predicting disability progression. A test-retest study was conducted with dynamic [11C]PiB PET to assess reproducibility in measuring these metrics, and to identify reliable biomarkers that can be used in clinical applications. The second axis of the thesis explores deep learning techniques to automatically segment and control the quality of CP volume measurements on T1-weighted MRI. The CPs, involved in neuroinflammatory responses, offer a promising biomarker for MS across different disease stages. By creating a robust, reproducible segmentation framework, this work enhances our ability to quantify CP volume changes accurately, providing insight into neuroinflammation associated with MS progression. Finally, the genetic architecture of CP volume is examined, focusing on the heritability of this phenotype and identifying genomic loci that may be associated with it. This research pinpoints significant loci linked to CP volume by using genome-wide association studies (GWAS) on MRI-derived phenotypes from the UK Biobank. Advanced genetic mapping techniques, polygenic risk scores, and LD score regression were employed to assess the genetic correlation of CP volume with other traits, offering a comprehensive view of the genetic factors influencing CP variability. In conclusion, this thesis represents an integrative approach to developing imaging and genomic biomarkers for exploring the pathophysiology of MS. By combining PET and MRI with advanced genetic analyses, it provides a multidimensional perspective on MS, identifying potential mechanisms underlying neurodegeneration and neuroinflammation. This integrative framework supports the development of targeted biomarkers that could improve diagnosis, monitoring, and therapeutic interventions

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Turcotte, Raphael. "Optical molecular structural imaging of myelin in a multiple sclerosis context: Polarization dependence coherent anti-Stokes Raman scattering microscopy." Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/28626/28626.pdf.

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Being able to visualize new pathogenic features is a gold standard in the biological imag- ing community. The principal goal of this master’s project is to develop a new optical microscopy modality capable of characterizing myelin molecular structural integrity in vivo. This tool is to be used in multiple sclerosis research. Using the polarization de- pendence of coherent anti-Stokes Raman scattering (CARS), we were able to quantify the degree of myelin ordering. Mapping this ordering for every pixels in an image results in molecular structural imaging. Optical molecular structural imaging is, to some ex- tent, similar to electron microscopy, but has the distinct advantage that it can be used on thick and live tissue which provides better context. The index describing myelin ordering is the amplitude modulation. After a full analysis of the amplitude modula- tion, myelin molecular structural imaging was used to study the EAE animal model of multiple sclerosis. A new type of focal myelin membrane disruption was identified. No other existing technique can describe the myelin molecular structure at such a large scale and in live biological tissue. Myelin molecular imaging was also applied to study the spinal cord development in zebrafish. We were able to quantitatively describe a fine but nonetheless generalized reorganization of the myelin sheath through early stages of development although no microscopic morphological changes were apparent. This capacity of observing subtle myelin modification will certainly reveal itself useful in the monitoring of remyelination.
Pouvoir visualiser de nouveaux éléments pathogéniques est un but standard dans la monde de l’imagerie médicale. L’objectif principal de ce projet de maîtrise est le développement d’une modalité en microscopie optique qui permet la caractérisation de l’intégrité de la structure moléculaire de la myéline in vivo. Cet outil sera utilisé pour la recherche sur la sclérose en plaques. En utilisant la dépendance en polarisation présente en diffusion Raman cohérente, nous avons été en mesure de quantifier le degré d’ordre de la myéline. Représenter cet ordre à tous les pixels d’une image résulte en imagerie de la structure moléculaire. L’imagerie de la structure moléculaire de la myé- line est similaire à la microscopie électronique, sauf qu’elle peut être appliquée sur des tissus biologiques épais et vivants. L’indice qui décrit l’organisation de la myéline est l’amplitude de modulation. L’imagerie de la structure moléculaire a été utilisée pour étudier le modèle animal EAE de la sclérose en plaques. Un nouveau type de lésions focales de la membrane de myéline a été identifié. Aucune autre technique existante permet une description de l’organisation moléculaire de la myéline à une si grande échelle dans du tissu vivant. L’imagerie de la structure moléculaire de la myéline a aussi été utilisée pour l’étude du développement de la moelle épinière de dard-perches (zebrafish), une espèce de poisson, et pour évaluer l’impact de certaines drogues sur ce dernier. Nous avons pu mesurer une fine, mais néanmoins généralisée, réorganisation de la membrane de myéline et ce malgré l’absence de modification morphologique. Cette capacité d’observer de subtiles modifications de la myéline se révélera certainement utile pour l’étude de la remyélinisation.

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Turcotte, Raphaël. "Optical molecular structural imaging of myelin in a multiple sclerosis context : polarization dependence coherent anti-Stokes Raman scattering microscopy." Master's thesis, Université Laval, 2011. http://hdl.handle.net/20.500.11794/23879.

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Pouvoir visualiser de nouveaux éléments pathogéniques est un but standard dans la monde de l’imagerie médicale. L’objectif principal de ce projet de maîtrise est le développement d’une modalité en microscopie optique qui permet la caractérisation de l’intégrité de la structure moléculaire de la myéline in vivo. Cet outil sera utilisé pour la recherche sur la sclérose en plaques. En utilisant la dépendance en polarisation présente en diffusion Raman cohérente, nous avons été en mesure de quantifier le degré d’ordre de la myéline. Représenter cet ordre à tous les pixels d’une image résulte en imagerie de la structure moléculaire. L’imagerie de la structure moléculaire de la myé- line est similaire à la microscopie électronique, sauf qu’elle peut être appliquée sur des tissus biologiques épais et vivants. L’indice qui décrit l’organisation de la myéline est l’amplitude de modulation. L’imagerie de la structure moléculaire a été utilisée pour étudier le modèle animal EAE de la sclérose en plaques. Un nouveau type de lésions focales de la membrane de myéline a été identifié. Aucune autre technique existante permet une description de l’organisation moléculaire de la myéline à une si grande échelle dans du tissu vivant. L’imagerie de la structure moléculaire de la myéline a aussi été utilisée pour l’étude du développement de la moelle épinière de dard-perches (zebrafish), une espèce de poisson, et pour évaluer l’impact de certaines drogues sur ce dernier. Nous avons pu mesurer une fine, mais néanmoins généralisée, réorganisation de la membrane de myéline et ce malgré l’absence de modification morphologique. Cette capacité d’observer de subtiles modifications de la myéline se révélera certainement utile pour l’étude de la remyélinisation.
Being able to visualize new pathogenic features is a gold standard in the biological imag- ing community. The principal goal of this master’s project is to develop a new optical microscopy modality capable of characterizing myelin molecular structural integrity in vivo. This tool is to be used in multiple sclerosis research. Using the polarization de- pendence of coherent anti-Stokes Raman scattering (CARS), we were able to quantify the degree of myelin ordering. Mapping this ordering for every pixels in an image results in molecular structural imaging. Optical molecular structural imaging is, to some ex- tent, similar to electron microscopy, but has the distinct advantage that it can be used on thick and live tissue which provides better context. The index describing myelin ordering is the amplitude modulation. After a full analysis of the amplitude modula- tion, myelin molecular structural imaging was used to study the EAE animal model of multiple sclerosis. A new type of focal myelin membrane disruption was identified. No other existing technique can describe the myelin molecular structure at such a large scale and in live biological tissue. Myelin molecular imaging was also applied to study the spinal cord development in zebrafish. We were able to quantitatively describe a fine but nonetheless generalized reorganization of the myelin sheath through early stages of development although no microscopic morphological changes were apparent. This capacity of observing subtle myelin modification will certainly reveal itself useful in the monitoring of remyelination.

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Damle, Sheela Ruby. "TYPE 2 IMMUNE RESPONSES IN THE CONTEXT OF HELMINTH INFECTION, ASTHMA, DENDRITIC CELLS, AND MYELOID DERIVED SUPPRESSOR CELL FUNCTION." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4696.

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Type 2 (TH2) immune responses evolved to respond to helminth parasite infections by the production of TH2 cytokines, which stimulate anti-helminth immunity. Macrophage migration inhibitor factor (MIF) is a pleiotropic cytokine, which is produced by many cell types. We demonstrate that mice deficient in MIF have enhanced clearance of a helminth parasite. MIF deficiency in CD4+ T cells was found to be the most important for mediating parasite clearance. We mimicked MIF deficiency by administering an inhibitor of the MIF tautomerase activity, sulforaphane, and this also increased parasite clearance (Section I). TH2 immune responses underlie allergy and allergic asthma, in which the same cytokines that help expel parasites are released in response to innocuous substances. Integral to the initiation of adaptive TH2 immunity are dendritic cells (DCs), which take up antigen and stimulate antigen-specific CD4+ T cell responses. We found that DC expression of ADAM10, a zinc-dependent metalloproteinase, is critical for the development of TH2 immune responses and IgE production from B cells. This effect is demonstrated in both allergic airway inflammation and anaphylaxis models. ADAM10-deficient DCs are unable to cleave Notch1 receptors, resulting in reduced IL-6 production and this ultimately results in decreased TH2 activity. ADAM17 is closely related to ADAM10 in both structure and function. Interestingly, mice from which ADAM10 and 17 are removed from DCs (ADAM10/17DC-/-) have a distinct phenotype from both ADAM10DC-/- and ADAM17DC-/- mice in models of allergic airway inflammation (Section I). We also examined another effect of TH2 cytokines on the interaction between mast cells and myeloid derived suppressor cells (MDSCs). We sought to understand how histamine and IL-13, mediators made by mast cells, affect the immunoregulatory function of MDSCs. MDSCs in IL-13-deficient mice with tumor are more prevalent in circulation rather than in tumor or organs, which could be due to changes in CCL2/CCR2 chemotaxis. In addition, MDSC function after treatment with the DNA methyltransferase inhibitor, decitabine was examined. This treatment reduced their suppressive function and increased the expression of molecules needed for antigen presentation. Overall, TH2 immunity has multifaceted roles in anti-parasite immunity, allergic asthma, and MDSC function (Section II).

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Zhang, Yu Wei. "H3K27M/I mutations promote context-dependent transformation in acute myeloid leukemia with RUNX1 alterations." Thèse, 2017. http://hdl.handle.net/1866/20402.

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Books on the topic "Myelin Content"

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B12 (cobalamin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0013.

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Vitamin B12 is required for the synthesis of fatty acids and myelin and so is crucial for normal neurological function and maintenance of the CNS. In conjunction with folate, it is involved in red blood cell formation and DNA synthesis, and in embryogenesis, it is important for proper neural tube formation and brain development. Maternal intake during pregnancy is important, as only newly absorbed vitamin B12, and not that stored in the maternal liver, is concentrated in the placenta. Despite the active transfer during pregnancy, the vitamin B12 content in the newborn is low, and the infant is dependent on breast milk for ongoing needs. Pregnant and lactating women should ensure that their diet contains sufficient (animal) sources of vitamin B12; those consuming vegan or strict vegetarian diets should either take vitamin B12 supplements or seek foods that have been fortified with vitamin B12.

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Karagiannis, George S., and Panagiota S. Filippou, eds. Revisiting the Metastatic Cascade: Putting Myeloid Cells Into Context. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-467-2.

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Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.

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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.

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Book chapters on the topic "Myelin Content"

Krupina, Ekaterina, Andrei Manzhurtsev, Maxim Ublinskiy, Larisa Mosina, Maria Osetrova, Vasily Yarnykh, Galina Mamedova, et al. "Preliminary Study of Cerebral Myelin Content Alterations at Schizophrenia." In Biologically Inspired Cognitive Architectures 2023, 485–94. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-50381-8_51.

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Wei, Wen, Emilie Poirion, Benedetta Bodini, Stanley Durrleman, Nicholas Ayache, Bruno Stankoff, and Olivier Colliot. "Learning Myelin Content in Multiple Sclerosis from Multimodal MRI Through Adversarial Training." In Medical Image Computing and Computer Assisted Intervention – MICCAI 2018, 514–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00931-1_59.

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Neuberger, Timothy J., and George H. De Vries. "Axonal Contact as a Determinant of Oligodendrocyte and Schwann Cell Function." In Myelin, 173–93. Boca Raton: Routledge, 2023. http://dx.doi.org/10.1201/9780203746141-6.

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Goujet-Zalc, C., C. Lubetzki, Ch Babinet, M. Monge, S. Timsit, C. Demerens, M. Miura, et al. "Axonal Contact Induces Oligodendroglial Specific Transcription of the MBP Gene from the Proximal Promoter Region." In A Multidisciplinary Approach to Myelin Diseases II, 23–28. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2435-9_3.

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Abdulaziz Othman Alkubaisi, Noorah, and Nagwa Mohammed Amin Aref. "Chloroplast and Mitochondria." In Atlas of Ultrastructure Interaction Proteome Between Barley Yellow Dwarf Virus and Gold Nanoparticles. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97440.

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Photosynthesis is a crucial process for plants on earth that changes light energy to chemical energy. Virus infection can cause dramatic photosynthesis changes: respiration and the translocation of carbohydrates and other substances around the host plant. Chlorosis in virus-infected leaves like Barley Yellow Dwarf Virus (BYDV- PAV).infection can result from damage to chloroplasts resulting from inhibition of photosynthetic activity. Our present study combines TEM and chlorophyll-level content in the presence of Gold nanoparticles (AuNPS) to explore the repair mechanism for the yellowing leaf symptom development caused by infection with BYDV- PAV by illustrating TEM micrographs; showing fragmentized grana, deformation of the myelin like bodies (MLB), many vesicles; osmiophilic lipid granules/plastoglobulus, starch body, and plasmolysis in the chloroplast, distribution of AuNPs & VLPs near and inside the chloroplast. Mitochondria, Double-membrane-bound organelle, Distorted mitochondrion, Amorphous inclusion bodies.

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"Contents of Recent Volumes." In Development and Function of Myeloid Subsets, 311–23. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-417028-5.09985-3.

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Benarroch, Eduardo E. "Microglia and Neuroinflammation." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 402–15. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0022.

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Microglia maintain cellular, synaptic, and myelin homeostasis during development and normal function and response to injury. Surveilling icroglia actively explore their environment by dynamically extending thin processes that respond to local signals. Activated (“reactive,” or “effector”) microglia constitute a heterogeneous population that dynamically change in phenotype depending on their environmental context and may mediate either injury or neuroprotection, repair, and circuit refinement. Any type of injury in the CNS elicits activation of microglia, astrocytes, and oligodendrocyte precursors, which together with infiltrating cells from the blood in the case of blood-brain barrier disruption interact via several signals to elicit elimination of pathogens, limit the spatial extent of the lesion, and eventually promote tissue remodeling, repair, and remyelination. Neuroinflammation is a feature of essentially all types of neurologic disorders, including traumatic, vascular, and inflammatory/demyelinating lesions; autoimmune encephalitis; and neurodegenerative disorders and has a major role in mechanisms of epilepsy and pain.

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Russell, Nigel, and Alan Burnett. "Acute myeloid leukaemia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5205–12. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0515.

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Acute myeloblastic leukaemia arises in a haematopoietic stem cell as a result of mutations which promote growth or inhibit apoptosis in association with mutations that inhibit differentiation. There is usually no obvious cause, but exposure to chemical and ionizing radiation may be relevant, including previous chemotherapy for solid tumours. This leukaemia arises particularly in older patients, often in the context of antecedent haematological disorders such as myelodysplastic syndromes or myeloproliferative neoplasms. Clinical features are of marrow failure, with anaemia, bleeding (petechiae, purpura, from mucous membranes), and infection. Acute promyelocytic leukaemia should be viewed as a medical emergency characterized by disseminated intravascular coagulation which requires urgent treatment to avoid haemorrhagic death. Aside from providing appropriate supportive care, the first clinical decision to be made is whether to give conventional intensive chemotherapy aiming for disease eradication, or to adopt a more palliative approach. Intensive chemotherapy is the norm up to age 65 to 70 years. Above this age, the biology of the disease tends to be less favourable and patients may have significant comorbidities limiting treatment tolerance. In patients under 60 years, 75 to 80% will achieve initial remission and about 45 to 50% will survive. In older patients given intensive treatment, 50 to 60% will enter remission but only 15 to 20% will survive 2 years. With nonintensive treatments, remissions are seen in 15 to 25% with the median survival being 6 to 9 months. Relapsed disease—more than 50% of patients will ultimately relapse and their overall outcome is generally very poor. The best curative option is allogeneic stem cell transplantation if a second complete remission can be achieved with reinduction chemotherapy.

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Zupanc, Günther K. H. "Fundamentals of neurobiology." In Behavioral Neurobiology. Oxford University Press, 2019. http://dx.doi.org/10.1093/hesc/9780198738725.003.0002.

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This chapter introduces the fundamentals of neurobiology, specifically the concepts and methodologies that are of immediate relevance to behavioral neurobiology. It discusses the cellular and subcellular composition of nervous systems – comparing cell theory and reticular theory. The discussion covers the Golgi method, an histological staining technique invented by Camillo Golgi, as well as the work of Spanish neurohistologist Santiago Ramón y Cajal who further improved the staining technique and applied it to many parts of the nervous system, providing strong evidence in support of cell theory. Furthermore, the chapter explains the salient features of neurons and nervous systems, the axons ensheathment by myelin, and the physiology and ionic basis of the electrical properties of neurons. It describes synapses, the specialized contact zones in the nervous system where a neuron communicates with another cell. The chapter also gives a glimpse of some neurobiological approaches in neuroethology.

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Padron, Eric, Tariq I. Mughal, David Sallman, and Alan F. List. "Myelodysplastic syndromes/myeloproliferative overlap neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms, 191–203. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0012.

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The myelodysplastic/myeloproliferative neoplasms (MDS/MPN) are haematologically diverse stem cell malignancies sharing phenotypic features of both myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN) that display a paradoxical bone marrow phenotype hallmarked by myeloid proliferation in the context of bone marrow dysplasia and ineffective haematopoiesis. The unfolding MDS/MPN genomic landscape has revealed numerous mutations in signalling genes, such as CBL, JAK2, NRAS, KRAS, CSF3R, and others involving the spliceosome complex. These observations suggest that comutation of genes involved in dysplasia and bone marrow failure along with those of cytokine receptor signalling may, in part, explain the dual MDS/MPN phenotype. The respective MDS/MPN diseases are identified by the type of myeloid subset which predominates in the peripheral blood. Currently there are no standard treatment recommendations for most patients with MDS/MPN. To optimize efforts to improve the management and disease outcomes, it is essential to identify meaningful clinical and biologic endpoints and standardized response criteria for clinical trials.

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Conference papers on the topic "Myelin Content"

Lee, Kevin, Marie Cherel, Francois Budin, John Gilmore, Kirsten Zaldarriaga Consing, Jerod Rasmussen, Pathik D. Wadhwa, et al. "Early postnatal myelin content estimate of white matter via T1w/T2w ratio." In SPIE Medical Imaging, edited by Barjor Gimi and Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2082198.

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Neves, Pedro Rodrigues, Daissy Liliana Mora Cuervo, Rafael Canani Sommer, Alessandra Jahn Gallo, Ana Djulia Tesche, Douglas Kazutoshi Sato, and Vitoria Pimentel. "Association between myelin content variation and clinico-radiological activity in multiple sclerosis." In 25th BCTRIMS Annual Meeting. Thieme Revinter Publicações Ltda., 2024. http://dx.doi.org/10.1055/s-0044-1789371.

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Chang, Shuaibin, Jiarui Yang, Anderson Chen, Sreekanth Kura, Caroline Magnain, Jean Augustinack, Divya Varadarajan, Bruce Fischl, David A. Boas, and Hui Wang. "Measuring myelin content and cell density in the human brain using optical coherence tomography." In Neural Imaging and Sensing 2021, edited by Qingming Luo, Jun Ding, and Ling Fu. SPIE, 2021. http://dx.doi.org/10.1117/12.2578489.

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Gallo, Alessandra, Giordani Rodrigues Dos Passos, Rafael Canani Sommer, Pedro Rodrigues Neves, Ana Djulia Tesche, Augusto Cesar Bressanim, Francisco Zuanazzi, et al. "Association of myelin content and neuropsychological tests with the risk of brain atrophy in multiple sclerosis." In 25th BCTRIMS Annual Meeting. Thieme Revinter Publicações Ltda., 2024. http://dx.doi.org/10.1055/s-0044-1789348.

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Soulier, Théodore, Mariem Hamzaoui, Milena Sales Pitombeira, Daniele De Paula Faria, Arya Yazdan-Panah, Matteo Tonietto, Claire Leroy, et al. "Generating PET-derived maps of myelin content from clinical MRI using curricular discriminator training in generative adversarial networks." In Image Processing, edited by Olivier Colliot and Jhimli Mitra. SPIE, 2024. http://dx.doi.org/10.1117/12.3004975.

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Chang, Shuaibin, Hui Wang, Jiarui Yang, Bruce Fischl, Shih-Chi Chen, David A. Boas, and Ichun Anderson Chen. "Concurrent imaging of large-scale vasculature, myelin content and cell density of post-mortem human brain with serial sectioning PSOCT-2PM." In Optical Coherence Tomography. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/oct.2022.cs4e.4.

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Chang, Shuaibin, Hui Wang, Jiarui Yang, Bruce Fischl, Shih-Chi Chen, Ann C. McKee, David A. Boas, and Ichun A. Chen. "Large-scale myelin content and cell body imaging of post-mortem human brain: application in the neurodegeneration study of Alzheimer’s disease (AD) and chronic traumatic encephalopathy (CTE)." In Neural Imaging and Sensing 2022, edited by Qingming Luo, Jun Ding, and Ling Fu. SPIE, 2022. http://dx.doi.org/10.1117/12.2610275.

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Santos, Mariana Bastos Rodrigues dos, Felipe dos Santos Souza, Pedro Felisberto Nogueira Viana Farah, Yasmim Evelyn Lisboa Barbosa, and Felipe Oliveira Costa. "Early diagnosis of RelapsingRemitting Multiple Sclerosis: a review of the bibliography from 2016 to 2021." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.203.

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Background: Multiple Sclerosis (MS) is a neurodegenerative disease of the Central Nervous System (CNS), which damages myelin and axons by interrupting or reducing the flow of information. Early diagnosis of MS is essential to slow disease progression. The last review of the McDonald criteria, which organize the diagnosis of MS, took place in 2017 and it is necessary to understand the evidence that emerged in this period. Objectives: Review the updates of the bibliography published between 2016 and 2021. Design and setting: Bibliographic review made in Rio de Janeiro, Brazil. Methods: This research was made from Pubmed database search with the descriptors “Multiple Sclerosis Relapsing-Remitting” and “Early Diagnosis” and the filters “free full text”, “english”, “Portuguese”, “5 years”, “humans”. The discarded articles did not contemplate the entire theme in the design, content or quality of publication. Results: Patients with the first clinical event suggesting MS that meet the criteria for space dissemination may be diagnosed with relapsing-remitting multiple sclerosis (RRMS) when oligoclonal bands in the cerebrospinal fluid are detected, while other methods such as infrared spectroscopy and diffusion tensor tractography still show many concomitant signs among the varieties of MS. Conclusions: Cerebrospinal fluid analysis is the most sensitive criterion for early diagnosis of RRMS.

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"PROINFLAMMATORY ACTIVATION SUPPRESSES TRAIL-INDUCED APOPTOSIS OF ACUTE MYELOID LEUKEMIA CELLS." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-329.

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The study of the mechanisms of resistance of AML cells to the action of antitumor immunity mediators remains an extremely urgent task. The paper describes a new mechanism of TRAIL resistance of AML cells based on proinflammatory cellular activation accompanied by changes in the surface expression of proapototic TRAIL receptors, the content of the FADD adaptive protein and antiapoptotic factors cFLIPS, Livin and cIAP2.

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Zhang, X. "Abstract SP161: Context-dependent functions and inter-tumoral heterogeneity of tumor-associated myeloid cells." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-sp161.

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