Academic literature on the topic 'Myelinated and unmyelinated gray matter'
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Journal articles on the topic "Myelinated and unmyelinated gray matter"
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Kordeli, E., J. Davis, B. Trapp, and V. Bennett. "An isoform of ankyrin is localized at nodes of Ranvier in myelinated axons of central and peripheral nerves." Journal of Cell Biology 110, no. 4 (1990): 1341–52. http://dx.doi.org/10.1083/jcb.110.4.1341.
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Two variants of ankyrin have been distinguished in rat brain tissue using antibodies: a broadly distributed isoform (ankyrinB) that represents the major form of ankyrin in brain and another isoform with a restricted distribution (ankyrinR) that shares epitopes with erythrocyte ankyrin. The ankyrinR isoform was localized by immunofluorescence in cryosections of rat spinal cord gray matter and myelinated central and peripheral nerves to: (a) perikarya and initial axonal segments of neuron cells, (b) nodes of Ranvier of myelinated nerve with no detectable labeling in other areas of the myelinated axons, and (c) the axolemma of unmyelinated axons. Immunogold EM on ultrathin cryosections of myelinated nerve showed that ankyrinR was localized on the cytoplasmic face of the axolemma and was restricted to the nodal and, in some cases, paranodal area. The major isoform of ankyrin in brain (ankyrinB) displayed a broad distribution on glial and neuronal cells of the gray matter and a mainly glial distribution in central myelinated axons with no significant labeling on the axolemma. These results show that (a) ankyrin isoforms display a differential distribution on glial and neuronal cells of the nervous tissue; (b) an isoform of ankyrin codistributes with the voltage-dependent sodium channel in both myelinated and unmyelinated nerve fibers. Ankyrin interacts in vitro with the voltage-dependent sodium channel (Srinivasan, Y., L. Elmer, J. Davis, V. Bennett, and K. Angelides. 1988. Nature (Lond.). 333:177-180). A specific interaction of an isoform of ankyrin with the sodium channel thus may play an important role in the morphogenesis and/or maintenance of the node of Ranvier.
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Triulzi, F., C. Baldoli, E. Bianchini, and C. Parazzini. "Ottimizzazione di un protocollo RM per lo studio dell'encefalo neonatale." Rivista di Neuroradiologia 10, no. 2_suppl (1997): 51. http://dx.doi.org/10.1177/19714009970100s218.
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A fast, high quality MR study protocol for the neonatal brain is proposed. It allows to achieve in little more than 4 minutes and an half a complete set of strong T2 and T1-weighted high quality images of the entire neonatal brain. To optimize the signal to noise ratio a circular polarized coil with a small diameter (20 cm) was used. For the T2-weighted sequence a fast spin-echo sequence with and echo train of 15, TR 5200 and TE 132 was performed, whereas a fast true inversion recovery with an echo train of 11 was utilized for the T1-weighted sequence. Field of view was mainly 130 mm for both sequences with a pixel size of 0,81times0,51 and 0,74times0,51 respectively. Up to now 30 patients were studied with this technique. The short total acquisition time allows more reliable studies in non sedated patients; the use of true inversion recovery sequence allows better contrast resolution between gray matter and unmyelinated white matter and between unmyelinated and myelinated white matter.
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Einheber, Steven, George Zanazzi, William Ching, et al. "The Axonal Membrane Protein Caspr, a Homologue of Neurexin IV, Is a Component of the Septate-like Paranodal Junctions That Assemble during Myelination." Journal of Cell Biology 139, no. 6 (1997): 1495–506. http://dx.doi.org/10.1083/jcb.139.6.1495.
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We have investigated the potential role of contactin and contactin-associated protein (Caspr) in the axonal–glial interactions of myelination. In the nervous system, contactin is expressed by neurons, oligodendrocytes, and their progenitors, but not by Schwann cells. Expression of Caspr, a homologue of Neurexin IV, is restricted to neurons. Both contactin and Caspr are uniformly expressed at high levels on the surface of unensheathed neurites and are downregulated during myelination in vitro and in vivo. Contactin is downregulated along the entire myelinated nerve fiber. In contrast, Caspr expression initially remains elevated along segments of neurites associated with nascent myelin sheaths. With further maturation, Caspr is downregulated in the internode and becomes strikingly concentrated in the paranodal regions of the axon, suggesting that it redistributes from the internode to these sites. Caspr expression is similarly restricted to the paranodes of mature myelinated axons in the peripheral and central nervous systems; it is more diffusely and persistently expressed in gray matter and on unmyelinated axons. Immunoelectron microscopy demonstrated that Caspr is localized to the septate-like junctions that form between axons and the paranodal loops of myelinating cells. Caspr is poorly extracted by nonionic detergents, suggesting that it is associated with the axon cytoskeleton at these junctions. These results indicate that contactin and Caspr function independently during myelination and that their expression is regulated by glial ensheathment. They strongly implicate Caspr as a major transmembrane component of the paranodal junctions, whose molecular composition has previously been unknown, and suggest its role in the reciprocal signaling between axons and glia.
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Uranova, Natalya A., Olga V. Vikhreva, Valentina I. Rachmanova, and Diana D. Orlovskaya. "Ultrastructural Alterations of Myelinated Fibers and Oligodendrocytes in the Prefrontal Cortex in Schizophrenia: A Postmortem Morphometric Study." Schizophrenia Research and Treatment 2011 (2011): 1–13. http://dx.doi.org/10.1155/2011/325789.
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Schizophrenia is believed to result from altered neuronal connectivity and impaired myelination. However, there are few direct evidence for myelin abnormalities in schizophrenia. We performed electron microscopic study of myelinated fibers and oligodendrocytes and morphometric study of myelinated fibers in the prefrontal cortex in gray and white matters in schizophrenia and normal controls. Six types of abnormal fibers and ultrastructural alterations of oligodendrocytes were found in schizophrenia. No significant group differences in area density of myelinated fibers were found. Frequency of pathological fibers was increased significantly in gray matter in young and elderly schizophrenia patients and in patients with predominantly positive symptoms. In contrast, in white matter, frequency of altered fibers was increased significantly in elderly patients, in patients with predominantly negative symptoms, and correlated with illness duration. Progressive alterations of myelinated fibers in white matter might be followed by alterations of myelinated fibers in gray matter in schizophrenia.
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Lee, CK, A. Alarfaj, J. Ai, B. Alharbi, P. Vasdev, and RL Macdonald. "Neurosurgery (Neuro Vascular)." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (2015): S48. http://dx.doi.org/10.1017/cjn.2015.216.
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Background: Blood breakdown products such as bilirubin and bilirubin oxidation products damage cortex and white matter after intracerebral hemorrhage(ICH). Here, we tested whether albumin can antagonize axonal damage caused by bilirubin. Methods: The effect of albumin on white matter injury was investigated using brain slices in vitro. After CD-1 mice brain slices were cut using a vibratome, they were incubated in one of five solutions: artificial cerebral spinal fluid (ACSF), bilirubin ACSF, bilirubin and albumin ACSF, bilirubin ACSF that had albumin added 1 hour(h) later, and bilirubin and denatured albumin ACSF. All solutions were continuously aerated with 95% O2 and 5% CO2. Subsequently, electrophysiological recordings of axonal response to electrical stimulation were performed 8h after incubation of brain slices. Results: Bilirubin treatment profoundly damaged both myelinated and unmeylinated axons in brain slices, but had a greater effect on myelinated axons. Unmyelinated axons were found to be more susceptible to damage from denatured albumin. Albumin treatment at 0 h and 1 h significantly diminished bilirubin toxicity for both myelinated and unmyelinated axons, with 1 h delayed albumin treatment conferring greater neuroprotection. Conclusions: These results implicate the role of albumin in preventing bilirubin-induced axonal damage following ICH and its potential therapeutic value for hemorrhagic stroke.
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Lakovic, Katarina, Jinglu Ai, Josephine D'Abbondanza, et al. "Bilirubin and its Oxidation Products Damage Brain White Matter." Journal of Cerebral Blood Flow & Metabolism 34, no. 11 (2014): 1837–47. http://dx.doi.org/10.1038/jcbfm.2014.154.
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Brain injury after intracerebral hemorrhage (ICH) occurs in cortex and white matter and may be mediated by blood breakdown products, including hemoglobin and heme. Effects of blood breakdown products, bilirubin and bilirubin oxidation products, have not been widely investigated in adult brain. Here, we first determined the effect of bilirubin and its oxidation products on the structure and function of white matter in vitro using brain slices. Subsequently, we determined whether these compounds have an effect on the structure and function of white matter in vivo. In all, 0.5 mmol/L bilirubin treatment significantly damaged both the function and the structure of myelinated axons but not the unmyelinated axons in brain slices. Toxicity of bilirubin in vitro was prevented by dimethyl sulfoxide. Bilirubin oxidation products (BOXes) may be responsible for the toxicity of bilirubin. In in vivo experiments, unmyelinated axons were found more susceptible to damage from bilirubin injection. These results suggest that unmyelinated axons may have a major role in white-matter damage in vivo. Since bilirubin and BOXes appear in a delayed manner after ICH, preventing their toxic effects may be worth investigating therapeutically. Dimethyl sulfoxide or its structurally related derivatives may have a potential therapeutic value at antagonizing axonal damage after hemorrhagic stroke.
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Evonuk, Kirsten S., Ryan E. Doyle, Carson E. Moseley, et al. "Reduction of AMPA receptor activity on mature oligodendrocytes attenuates loss of myelinated axons in autoimmune neuroinflammation." Science Advances 6, no. 2 (2020): eaax5936. http://dx.doi.org/10.1126/sciadv.aax5936.
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Glutamate dysregulation occurs in multiple sclerosis (MS), but whether excitotoxic mechanisms in mature oligodendrocytes contribute to demyelination and axonal injury is unexplored. Although current treatments modulate the immune system, long-term disability ensues, highlighting the need for neuroprotection. Glutamate is elevated before T2-visible white matter lesions appear in MS. We previously reported that myelin-reactive T cells provoke microglia to release glutamate from the system xc− transporter promoting myelin degradation in experimental autoimmune encephalomyelitis (EAE). Here, we explore the target for glutamate in mature oligodendrocytes. Most glutamate-stimulated calcium influx into oligodendrocyte somas is AMPA receptor (AMPAR)–mediated, and genetic deletion of AMPAR subunit GluA4 decreased intracellular calcium responses. Inducible deletion of GluA4 on mature oligodendrocytes attenuated EAE and loss of myelinated axons was selectively reduced compared to unmyelinated axons. These data link AMPAR signaling in mature oligodendrocytes to the pathophysiology of myelinated axons, demonstrating glutamate regulation as a potential neuroprotective strategy in MS.
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Bellani, Marcella, Carlo Alberto Marzi, and Paolo Brambilla. "Interhemispheric communication in schizophrenia." Epidemiologia e Psichiatria Sociale 18, no. 1 (2009): 19–22. http://dx.doi.org/10.1017/s1121189x0000141x.
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The corpus callosum (CC) is the brain's largest white matter tract, mostly composed by both myelinated and unmyelinated fibres, connecting the two cerebral hemispheres. The CC can be divided into different sections: rostrum, genu, body, isthmus and splenium (Aboitiz et al., 1992). Myelinated fibres predominate in the midbody and the splenium while unmyelinated fibres are more numerous in the rostrum and the genu. The callosal fiber disposition approximately reflects brain topography: the anterior sections connect the frontal lobes, the median sections connect temporal and parietal regions, and the posterior sections link occipital areas (Pandya et al., 1971). This traditional picture, however, which has been obtained mainly through studies in non-human primates has been partly modified by modern diffusion tensor imaging studies in humans (Hofer & Frahm, 2006). The CC matures after birth through adolescence and into early adulthood and is involved in different cognitive processes such as sensory-motor integration, attention, language, arousal and memory. Its size has been shown to be associated with handedness, sex (i.e., greater splenium in females and greater genu in males, Dubb et al., 2003) and cerebral laterality (i.e., inverse correlation between callosal connectivity and brain lateralization in males; Luders et al., 2003), and age (Ota et al., 2006) Specifically, age-related callosal degeneration has been detected by a diffusion tensor imaging (DTI) study (Ota et al., 2006) in the sub-regions that connect areas which are thought to be vulnerable to normal aging: the genu, rostral body, and isthmus. This result replicated post mortem findings of callosal degeneration in rostral body, anterior midbody and isthmus (Aboitiz et al., 1996).
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Miles, Lili, Ton J. deGrauw, Argirios Dinopoulos, Kim M. Cecil, Marjo S. van der Knaap, and Kevin E. Bove. "Megalencephalic Leukoencephalopathy with Subcortical Cysts: A Third Confirmed Case with Literature Review." Pediatric and Developmental Pathology 12, no. 3 (2009): 180–86. http://dx.doi.org/10.2350/08-06-0481.1.
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Megalencephalic leukoencephalopathy with subcortical cysts (MLC) causes early-onset, slowly progressive central nervous system white matter disease, macrocephaly, and later cognitive and motor decline. We describe brain structure in a patient with MLC and proven MLC1 mutations. A male, normal at birth, had macrocephaly at 6 months followed by developmental delay. Magnetic resonance imaging showed extensive signal abnormality in cerebral white matter and subcortical progressive cystic changes in the bilateral temporal and right frontal areas. Biopsy of frontal gyrus at age 15 months showed normal gray matter. The subcortical white matter was pale due to prominent fine uniform 2- to 4-μ-thick vacuoles with a few interspersed myelinated axons and rare microglia. The vacuoles had a single-, double-, or, rarely, triple-unit membrane (resembling myelin) and contained occasional organelles but no intermediate filaments. Both normal myelinated and thinly myelinated axons were observed. The outer and occasionally the inner layers of myelin surrounding intact axons formed blebs that may represent a source for vacuoles. Genetic analysis identified 2 heterozygous mutations of intron 3 (c.322–1 G>A) and intron 7 (c.597+1G>A), the 1st leading to deletion of amino acids 60 to 89 and the 2nd to deletion of amino acids 194 to 199. Fine uniform vacuolation of white matter with wide separation of myelinated axons is the hallmark of MLC in early childhood.
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Cammer, W., R. Sacchi, and V. Sapirstein. "Immunocytochemical localization of carbonic anhydrase in the spinal cords of normal and mutant (shiverer) adult mice with comparisons among fixation methods." Journal of Histochemistry & Cytochemistry 33, no. 1 (1985): 45–54. http://dx.doi.org/10.1177/33.1.3917467.
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The peroxidase-antiperoxidase technique was used for immunocytochemical localization of carbonic anhydrase in the mouse spinal cord to detect whether this antigen was normally present in myelinated fibers, in oligodendrocytes in both white and gray matter, and in astrocytes, and to determine where the carbonic anhydrase might be localized in the spinal cords of dysmyelinating mutant (shiverer) mice. The most favorable methods for treating tissue were: 1) immersion in formalin-ethanol-acetic acid followed by paraffin embedding, or 2) light fixation with paraformaldehyde and preparation of vibratome sections. Carnoy's solution, followed by paraffin embedding, extracted myelin from the tissue, while aqueous aldehydes, when used before paraffin embedding, reduced staining everywhere except at sites of compact myelin. The latter conclusion was based, in part, on the almost complete loss of this antigen from the shiverer cord, where compact myelin is known to be virtually absent but where membrane-bound carbonic anhydrase was demonstrated enzymatically. When the optimal methods were used with normal mouse cords, carbonic anhydrase was found throughout the white matter columns and in the oligodendrocytes in gray and white matter. The staining of the white matter was attributed to myelinated fibers because of the similarity in distribution to both a histological myelin stain and the immunocytochemical staining for myelin basic protein. In the mutant mice the oligodendrocyte cell bodies and processes, which were stained in all areas of the spinal cord, were particularly numerous at the periphery of the sections. In contrast to the oligodendrocytes, the fibrous astrocytes appeared to lack carbonic anhydrase, or to have lower than detectable levels, since the astrocyte marker, glial fibrillary acidic protein, had a very different distribution from that of carbonic anhydrase. Even finer localization was obtained in vibratome sections, where the antibody against carbonic anhydrase permitted visualization of the processes connecting oligodendrocytes to myelinated fibers in the normal adult spinal cord.
Dissertations / Theses on the topic "Myelinated and unmyelinated gray matter"
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Kundu, Madan Gopal. "Advanced Modeling of Longitudinal Spectroscopy Data." Thesis, 2014. http://hdl.handle.net/1805/5454.
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Indiana University-Purdue University Indianapolis (IUPUI)<br>Magnetic resonance (MR) spectroscopy is a neuroimaging technique. It is widely used to quantify the concentration of important metabolites in a brain tissue. Imbalance in concentration of brain metabolites has been found to be associated with development of neurological impairment. There has been increasing trend of using MR spectroscopy as a diagnosis tool for neurological disorders. We established statistical methodology to analyze data obtained from the MR spectroscopy in the context of the HIV associated neurological disorder. First, we have developed novel methodology to study the association of marker of neurological disorder with MR spectrum from brain and how this association evolves with time. The entire problem fits into the framework of scalar-on-function regression model with individual spectrum being the functional predictor. We have extended one of the existing cross-sectional scalar-on-function regression techniques to longitudinal set-up. Advantage of proposed method includes: 1) ability to model flexible time-varying association between response and functional predictor and (2) ability to incorporate prior information.
Second part of research attempts to study the influence of the clinical and demographic factors on the progression of brain metabolites over time. In order to understand the influence of these factors in fully non-parametric way, we proposed LongCART algorithm to construct regression tree with longitudinal data. Such a regression tree helps to identify smaller subpopulations (characterized by baseline factors) with differential longitudinal profile and hence helps us to identify influence of baseline factors. Advantage of LongCART algorithm includes: (1) it maintains of type-I error in determining best split, (2) substantially reduces computation time and (2) applicable even observations are taken at subject-specific time-points.
Finally, we carried out an in-depth analysis of longitudinal changes in the brain metabolite concentrations in three brain regions, namely, white matter, gray matter and basal ganglia in chronically infected HIV patients enrolled in HIV Neuroimaging Consortium study. We studied the influence of important baseline factors (clinical and demographic) on these longitudinal profiles of brain metabolites using LongCART algorithm in order to identify subgroup of patients at higher risk of neurological impairment.<br>Partial research support was provided by the National Institutes of Health grants U01-MH083545, R01-CA126205 and U01-CA086368
Book chapters on the topic "Myelinated and unmyelinated gray matter"
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Reeves, Thomas M., Adele E. Doperalski, and Linda L. Phillips. "Unmyelinated and Myelinated Axons Exhibit Differential Injury and Treatment Responses Following Traumatic Injury." In White Matter Injury in Stroke and CNS Disease. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9123-1_15.
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Carter, Jonathan L., and J. Clarke Stevens. "Somatosensory Evoked Potentials." In Clinical Neurophysiology. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780195385113.003.0018.
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SEPs recorded with surface electrodes represent volume-conducted activity arising from myelinated peripheral and central axons, synapses in central gray matter, and changes in the size and shape of the volume conductor. They provide an objective measure of function in large-diameter myelinated sensory afferents peripherally and in proprioceptive pathways centrally. Changes in amplitude and latency can be used to localize lesions in the nervous system, to identify objectively abnormalities in patients with few sensory manifestations or none at all, and to monitor function over time.
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Cajal, S. Ramón Y., DR L. Azoulay, Neely swanson, and larry W. Swanson. "The Spinal Cord." In Histology Of The Nervous System. Oxford University PressNew York, NY, 1995. http://dx.doi.org/10.1093/oso/9780195074017.003.0010.
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Abstract We have now reviewed the most important features of cell types that form neural tissue. Our next task will be to consider the special area dealing with the organs formed by these cells, which are referred to as neural centers. All neural centers consist of two tissues or substances that differ in appearance and color; one is referred to as white matter and the other as gray matter. White matter is made up of myelinated axons and glial cells with lengthy processes, whereas gray matter consists of neurons that are intermingled to a greater or lesser extent with nerve fibers and glial cells having rather shorter processes.
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Cajal, S. Ramón Y., DR L. Azoulay, Neely swanson, and larry W. Swanson. "Commissural And Funicular Neurons." In Histology Of The Nervous System. Oxford University PressNew York, NY, 1995. http://dx.doi.org/10.1093/oso/9780195074017.003.0013.
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Abstract Cells in the gray matter of the spinal cord that we have referred to as ventral commissural neurons are characterized by an axon that courses ventrally and then transversely to cross the midline near the ventral, white commissure before entering the ventral funiculus on the opposite side of the cord and becoming one of the myelinated fibers in what we have called the commissural fascicle. Golgi was the first to demonstrate that these neurons send an axon to the ventral funiculus, and this projection has since been described in greater detail by ourselves, Kolliker, Van Gehuchten, Cl. Sala, Lenhossek, and Retzius.
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Goldberg, Elkhonon. "Architecture of the Brain:." In The New Executive Brain. Oxford University PressNew York, NY, 2009. http://dx.doi.org/10.1093/oso/9780195329407.003.0004.
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Abstract The brain consists of hundreds of billions of cells (neurons and glial cells), intricately interconnected by pathways (dendrites and axons). Several types of neurons and glial cells exist. Some of the pathways between neurons are local, branching within their immediate “neighborhoods.” But others are long, interconnecting distant neural structures. These long pathways are covered with white fatty tissue, myelin, which facilitates the passage of the electric signals generated within the neurons (action poten-tials). The neurons and short local connections together comprise the gray matter, and the long myelinated pathways comprise the white matter. Every neuron is interconnected with a myriad of other neurons, resulting in intricate patterns of interactions. Thus a network of mind-boggling complexity is constructed of relatively simple elements. The principle of achieving great complexity through multiple permutations of simple elements appears to be universal and is implemented in nature (and culture) in a variety of ways. Think, for instance, of language, in which thousands of words, sentences, and narratives are constructed out of a few dozen letters; or think of the genetic code—a virtually infinite number of variants can be achieved through the combination of a finite number of genes.
Conference papers on the topic "Myelinated and unmyelinated gray matter"
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Novoseltseva, Anna, Ting Xie, and Irving J. Bigio. "Extracting 3D Information from Widefield Birefringence Microscopy Images of Sparse Myelinated Fibers in Human Brain Gray Matter." In Clinical and Translational Biophotonics. Optica Publishing Group, 2024. http://dx.doi.org/10.1364/translational.2024.js4a.41.
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We report the application of widefield birefringence microscopy for 3D rendering of sparse myelinated fibers in human brain gray matter. This inexpensive and simple method offers the potential to inform studies of the brain connectome.