Relevant bibliographies by topics / Spinal cord Axons Oligodendroglia

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Spinal cord Axons Oligodendroglia'

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Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Spinal cord Axons Oligodendroglia"

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Furlan, JC, Y. Liu, W. Dietrich, MD Norenberg, S. Croul, and MG Fehlings. "CNS/CSCN Chair’s Select Abstract Presentations." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (May 2015): S9. http://dx.doi.org/10.1017/cjn.2015.68.

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Background: This study examines whether age is a key determinant for inflammatory response, oligodendroglial apoptosis and axonal survival after traumatic spinal cord injury (SCI). Methods: This study includes post-mortem spinal cord tissue from 64 cases of SCI (at cervical or high-thoracic level) and 38 controls cases. Each group was subdivided into younger and elderly individuals (≥65 years). Alternating sections from 2 to 3 segments caudal to SCI and age/sex/level-matched segments from controls were stained for: (i) neuroinflammation (neutrophils, macrophages, lymphocytes); (ii) apoptotic oligodendrocytes; (iii) axons; (iv) extent of degeneration. The number of cells or axons was counted in the motor and sensory areas within the spinal cord using unbiased stereological techniques. Results: Younger and elderly individuals had statistically similar number of inflammatory cells in most of the stages post-SCI. Younger and elderly individuals had similar number of oligodendrocytes in apoptosis in all stages following SCI. The number of preserved axons did not significantly differ between younger and elderly individuals with SCI and without prior CNS injury. Extend of degeneration within the spinal cord white matter did not significantly differ between the two groups. Conclusions: Our results indicate that age at the time of injury does not adversely affect the cellular inflammatory response, oligodendroglial apoptosis and axonal survival after traumatic SCI.
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Bondan, Eduardo Fernandes, Maria Anete Lallo, Maria de Fátima Monteiro Martins, and Dominguita Luhers Graça. "Schwann cell expression of an oligodendrocyte-like remyelinating pattern after ethidium bromide injection in the rat spinal cord." Arquivos de Neuro-Psiquiatria 68, no. 5 (October 2010): 783–87. http://dx.doi.org/10.1590/s0004-282x2010000500021.

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Schwann cells are recognized by their capacity of producing single internodes of myelin around axons of the peripheral nervous system. In the ethidium bromide (EB) model of primary demyelination in the brainstem, it is observed the entry of Schwann cells into the central nervous system in order to contribute to the myelin repair performed by the oligodendrocytes that survived to the EB gliotoxic action, being able to even remyelinate more than one axon at the same time, in a pattern of repair similar to the oligodendroglial one. The present study was developed in the spinal cord to observe if Schwann cells maintained this competence of attending simultaneously different internodes. It was noted that, on the contrary of the brainstem, Schwann cells were the most important myelinogenic cells in the demyelinated site and, although rare, also presented the capacity of producing more than one internode of myelin in distinct axons.
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Tsata, Vasiliki, Volker Kroehne, Daniel Wehner, Fabian Rost, Christian Lange, Cornelia Hoppe, Thomas Kurth, et al. "Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord." Development 147, no. 24 (November 6, 2020): dev193946. http://dx.doi.org/10.1242/dev.193946.

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ABSTRACTSpinal cord injury (SCI) results in loss of neurons, oligodendrocytes and myelin sheaths, all of which are not efficiently restored. The scarcity of oligodendrocytes in the lesion site impairs re-myelination of spared fibres, which leaves axons denuded, impedes signal transduction and contributes to permanent functional deficits. In contrast to mammals, zebrafish can functionally regenerate the spinal cord. Yet, little is known about oligodendroglial lineage biology and re-myelination capacity after SCI in a regeneration-permissive context. Here, we report that, in adult zebrafish, SCI results in axonal, oligodendrocyte and myelin sheath loss. We find that OPCs, the oligodendrocyte progenitor cells, survive the injury, enter a reactive state, proliferate and differentiate into oligodendrocytes. Concomitantly, the oligodendrocyte population is re-established to pre-injury levels within 2 weeks. Transcriptional profiling revealed that reactive OPCs upregulate the expression of several myelination-related genes. Interestingly, global reduction of axonal tracts and partial re-myelination, relative to pre-injury levels, persist at later stages of regeneration, yet are sufficient for functional recovery. Taken together, these findings imply that, in the zebrafish spinal cord, OPCs replace lost oligodendrocytes and, thus, re-establish myelination during regeneration.
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Casha, S., W. R. Yu, and M. G. Fehlings. "Oligodendroglial apoptosis occurs along degenerating axons and is associated with FAS and p75 expression following spinal cord injury in the rat." Neuroscience 103, no. 1 (February 2001): 203–18. http://dx.doi.org/10.1016/s0306-4522(00)00538-8.

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Grieb, Paweł, Maciej Świątkiewicz, Agnieszka Kamińska, Anselm Jünemann, Robert Rejdak, and Konrad Rejdak. "Citicoline: A Candidate for Adjunct Treatment of Multiple Sclerosis." Pharmaceuticals 14, no. 4 (April 2, 2021): 326. http://dx.doi.org/10.3390/ph14040326.

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In remitting–relapsing multiple sclerosis (RR-MS), relapses are driven by autoreactive immune cells that enter the brain and spinal cord and damage myelin sheaths of axons in white and grey matter, whereas during remissions myelin is repaired by activated oligodendroglial cells. Disease-modifying therapies (DMTs) may either retard/attenuate myelin damage or promote/enhance/speed up myelin repair. Almost all currently approved DMTs inhibit myelin damage and are considerably toxic. Enhancement of myelin repair is considered an unmet medical need of MS patients. Citicoline, known for many years as a nootropic and neuroprotective drug and recently pronounced food supplement, has been found to be significantly efficacious in two complementary rodent models of MS, experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced myelin toxicity. Moreover, citicoline treatment improves visual evoked potentials (VEPs) in glaucoma patients, which is relevant because VEP monitoring is frequently used as an indicator of remyelination in MS. Although over-the-counter availability of citicoline may impede its formal translation to the clinic of MS, evaluation of its efficacy for supporting remyelination in this disease is strongly indicated.
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Dowding, A. J., and J. Scholes. "Lymphocytes and macrophages outnumber oligodendroglia in normal fish spinal cord." Proceedings of the National Academy of Sciences 90, no. 21 (November 1, 1993): 10183–87. http://dx.doi.org/10.1073/pnas.90.21.10183.

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Duval, Tanguy, Ariane Saliani, Harris Nami, Antonio Nanci, Nikola Stikov, Hugues Leblond, and Julien Cohen-Adad. "Axons morphometry in the human spinal cord." NeuroImage 185 (January 2019): 119–28. http://dx.doi.org/10.1016/j.neuroimage.2018.10.033.

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Kanno, Takeshi, Tetsuro Kurotaki, Naoaki Yamada, Kotaro Yamashita, Yumi Wako, and Minoru Tsuchitani. "Activity of 2′, 3′-Cyclic Nucleotide 3′-Phosphodiesterase (CNPase) in Spinal Cord with Spongy Change Induced by a Single Oral Dose of Aniline in Rats." Toxicologic Pathology 38, no. 3 (March 16, 2010): 359–65. http://dx.doi.org/10.1177/0192623310362245.

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A spongy change in the spinal cord white matter was observed in four-week-old rats treated with aniline. Although this change was found to be a result of the myelin sheath splitting at the ultrastructural level, the mechanism is unknown. This study was conducted to identify the mechanism of the spongy change in aniline-treated rats. The spongy change in the spinal cord white matter was first detected on day 5 in the histopathologic examination. The incidence and severity of the lesions, especially in the lateral and ventral funiculi of the thoracic spinal cord white matter, increased prominently from day 8 to day 10. In all rats, immunohistochemical staining by anti-2′, 3′-cyclic nucleotide 3′-phosphodiesterase (CNPase) occurred along the cytoplasmic boundaries of the normal oligodendroglia. However, mild to moderate anti-CNPase staining extended to the swollen cytoplasm of the oligodendroglia in the aniline-treated rats from day 2 to day 4. In the electron microscopic examination, free ribosomes and rough endoplasmic reticula in the cytoplasm of the oligodendroglia increased on days 3 and 4. These changes were considered to be related to CNPase expression. However, CNPase expression decreased, whereas the spongy changes were detected from day 5. The reduction in CNPase expression may contribute to the changes in the myelin morphology observed in aniline intoxication.
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Svanidze, I. K., and D. P. Museridze. "Growth of axons in organotypical spinal cord culture." Bulletin of Experimental Biology and Medicine 109, no. 2 (February 1990): 232–35. http://dx.doi.org/10.1007/bf00841682.

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Holley, John A., and Jerry Silver. "Growth pattern of pioneering chick spinal cord axons." Developmental Biology 123, no. 2 (October 1987): 375–88. http://dx.doi.org/10.1016/0012-1606(87)90396-4.

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Dissertations / Theses on the topic "Spinal cord Axons Oligodendroglia"

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Sun, Fang. "Investigation of the stimuli inducing delayed oligodendrocyte apoptosis after rat spinal cord contusion injury." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148493870.

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Zhang, Lei. "Axonal regeneration of descending brain neurons in larval lamprey /." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9964016.

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Kikukawa, Soki. "Regeneration of dorsal column axons after spinal cord injury in young rats." Kyoto University, 1999. http://hdl.handle.net/2433/181700.

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要旨pdfファイル:タイトル「幼若ラットにおける脊髄損傷後の索路の再生」
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第7731号
医博第2084号
新制||医||708(附属図書館)
UT51-99-G325
京都大学大学院医学研究科脳統御医科学系専攻
(主査)教授 金子 武嗣, 教授 柴崎 浩, 教授 川口 三郎
学位規則第4条第1項該当
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Anderson, Emma S. "The Type IV Oligodendrocyte : experimental studies on chicken white matter /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med720s.pdf.

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Mather, Nicole K. "The development of the major brainstem decussations." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365330.

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Meacham, Kathleen Williams. "Selective surface activation of motor circuitry in the injured spinal cord." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/26571.

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Thesis (Ph.D)--Biomedical Engineering, Georgia Institute of Technology, 2009.
Committee Co-Chair: Shawn Hochman; Committee Co-Chair: Stephen P. DeWeerth; Committee Member: Lena Ting; Committee Member: Robert J. Butera; Committee Member: Robert Lee; Committee Member: Vivian K. Mushahwar. Part of the SMARTech Electronic Thesis and Dissertation Collection.
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Gannon, Sean Michael. "Plasticity in the intermediolateral cell column of the spinal cord following injury to sympathetic postganglionic axons." Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1407112137.

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Kullberg, Susanna. "On age related changes in axons and glia of the central nervous system /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-271-x/.

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Sayer, Faisal T. "Neurotrophins reduce degeneration of dorsal column sensory and corticospinal motor axons, but not secondary spinal cord damage." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0034/MQ66603.pdf.

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Kataoka, Kazuya. "Alginate, a bioresorbable material derived from brown seaweed, enhances elongation of amputated axons of spinal cord in infant rats." Kyoto University, 2004. http://hdl.handle.net/2433/147554.

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Books on the topic "Spinal cord Axons Oligodendroglia"

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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 "Spinal cord Axons Oligodendroglia"

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Waxman, Stephen G., and J. D. Kocsis. "Experimental Approaches to Restoration of Function of Ascending and Descending Axons in Spinal Cord Injury." In Neurobiology of Spinal Cord Injury, 215–39. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-200-5_10.

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de la Torre, J. C., and H. S. Goldsmith. "Can transected spinal cord axons be bribed into regeneration?" In The Omentum, 63–73. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3436-4_5.

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y Cajal, Santiago Ramón. "Neurons with Somata Outside the Spinal Cord Sending Axons to the Cord." In Texture of the Nervous System of Man and the Vertebrates, 367–403. Vienna: Springer Vienna, 1999. http://dx.doi.org/10.1007/978-3-7091-6435-8_15.

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Micevych, Paul E., Barbara E. Rodin, and Lawrence Kruger. "The Controversial Nature of the Evidence for Neuroplasticity of Afferent Axons in the Spinal Cord." In Spinal Afferent Processing, 417–43. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-4994-5_17.

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Itoh, Yasunobu, A. Tessler, M. Kowada, and M. Pinter. "Electrophysiological Responses in Foetal Spinal Cord Transplants Evoked by Regenerated Dorsal Root Axons." In Advances in Stereotactic and Functional Neurosurgery 10, 24–26. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9297-9_5.

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Guth, L., Ch P. Barrett, and E. J. Donati. "Histological Factors Influencing the Growth of Axons into Lesions of the Mammalian Spinal Cord." In Processes of Recovery from Neural Trauma, 271–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70699-8_24.

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Itoh, Yasunobu, M. Kowada, and A. Tessler. "Regeneration of Adult Dorsal Root Axons into Transplants of Dorsal or Ventral Half of Foetal Spinal Cord." In Advances in Stereotactic and Functional Neurosurgery 10, 20–23. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9297-9_4.

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Koch, Jan Christoph, Vinicius Toledo Ribas, and Paul Lingor. "Autophagy in the Degeneration of Optic Nerve and Spinal Cord Axons." In Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging, 197–211. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-805421-5.00010-0.

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Shinoda, Y., T. Ohgaki, T. Futami, and Y. Sugiuchi. "Chapter 2 Vestibular projections to the spinal cord: the morphology of single vestibulospinal axons." In Progress in Brain Research, 17–27. Elsevier, 1988. http://dx.doi.org/10.1016/s0079-6123(08)64488-x.

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Douglas, Kenneth. "Innervation." In Bioprinting, 77–97. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.003.0006.

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Abstract: This chapter informs the reader of the discovery of nerve growth factor, how it plays an important role in bioprinting by directing the growth of the axons of nerve cells along specific paths to repair peripheral nerve injuries, and of the nascent efforts in bioprinting spinal cord scaffolds that may aid in the repair of spinal cord injuries. The chapter apprises the reader of the glial family of cells that provide myelination (insulation) for nerves in the central nervous system. Glial cells are as numerous in the central nervous system (i.e., the brain and spinal cord) as neurons (nerve cells). The chapter also explains fluorescently tagged calcium ion flow within bioprinted nerve tissue. Intracellular calcium—calcium within cells—controls key cellular functions in all types of neurons. For example, nerve cells cause a release of calcium ions that initiate muscle contraction.
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Conference papers on the topic "Spinal cord Axons Oligodendroglia"

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Khan, Dauzvardis, and Sayers. "Carbon Filament Implants Used As A Substrate For Regenerating Spinal Cord Axons." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.593798.

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Khan, Talat, Michael Dauzvardis, and Scott Sayers. "Carbon filament implants used as a substrate for regenerating spinal cord axons." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761698.

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Shreiber, David I., Hailing Hao, and Ragi A. I. Elias. "The Effects of Glia on the Tensile Properties of the Spinal Cord." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190184.

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Glia, the primary non-neuronal cells of the central nervous system, were initially believed to bind or glue neurons together and/or provide a supporting scaffold [1, 2]. It is now recognized that these cells provide specialized and essential biological and regulatory functions. Still, their contributions to the overall mechanical properties would also strongly influence the tissue’s tolerance to loading conditions experienced during trauma and potentially regulate of function and growth in neurons and glia [3, 4]. White matter represents an intriguing tissue to appreciate the role of glia in tissue and cellular mechanics. White matter consists of bundles of axons aligned in parallel, which are myelinated by oligodendrocytes, and a network of astrocytes, which interconnect axons and the vascular supply. In this study, we selectively interfered with the glial network during chick embryo development and evaluated the tensile properties of the spinal cord. Myelination was suppressed by injecting ethidium bromide (EB), which is cytotoxic to dividing cells and kills oligodendrocytes and astrocytes, or an antibody against galactocerebroside (αGalC) with serum complement, which interferes with oligodendrocytes during the myelination process without affecting astrocytes.
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Fournier, Adam, Suneil Hosmane, and K. T. Ramesh. "Thresholds for Embryonic CNS Axon Integrity, Degeneration, and Regrowth Using a Focal Compression Platform." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80331.

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Traumatic axonal injuries (TAI) are broadly defined as the focal or multi-focal damage of axons within white matter tracts of the central nervous system (CNS), and can occur in the setting of spinal cord injury (SCI) and traumatic brain injury (TBI). TAI can result from mechanical forces associated with the rapid deformation of white matter regions during trauma. Through combinations of compression, stretch, and shear, axon injury often results in an irreversible loss of functional neural connectivity, since the scope for axonal regeneration in the CNS is extremely limited.
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Long, Yu, Changhong Zhang, Ning Zhang, Yong Huang, and Xuejun Wen. "Formation of Highly Aligned Grooves on the Inner Surface of Semi-Permeable Hollow Fiber Membrane for the Directional Axonal Outgrowth." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-81235.

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It is generally believed that organized neural architecture is essential for both nervous system development, function, and regeneration. In the absence of guidance cues, regenerating axons may lose their directions and become misaligned, resulting in the formation of neuromas and/or misappropriate connections. To help regenerate axons across damaged regions and guide them to appropriate targets, some bridging devices such as microgrooves are being intensively researched to achieve a better directional axonal growth. This paper reports a novel fabrication process to generate a highly aligned groove texture on the inner surface of semi-permeable hollow fiber membranes (HFMs). HFMs were shown to be one of the most promising results in guiding axonal regeneration [1]. The fabrication process utilized a wet phase inversion procedure with polyurethane as model polymer, dimethyl sulfoxide (DMSO) as solvent, and water as nonsolvent. Data indicated that highly aligned groove texture could be formed on the HFM inner surface by carefully controlling phase inversion conditions such as the polymer solution flow rate, and/or nonsolvent flow rate, and/or polymer solution concentration ratio. The texture forming mechanism is qualitatively explained using a polyurethane (PU)-DMSO-water ternary phase diagram and the process dynamics. Axonal outgrowth on the HFM with aligned grooves showed the highly aligned orientation and improved axonal outgrowth length. This study will eventually lead to a new and effective way to engineer nerve grafts based on a highly aligned three dimensional scaffold for the spinal cord injury and nerve damage treatment.
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Pan, Yi, Vivak Patel, Assimina A. Pelegri, and David I. Shreiber. "Pseudo 3D RVE Based Finite Element Simulation on White Matter." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-89808.

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Axonal injury represents a critical target for traumatic brain and spinal cord injuries prevention and treatment. Finite element head models are often used to predict brain injury caused by mechanical loading exerted on the head. Many studies have been attempted to understand injury mechanisms and to define mechanical parameters of axonal injury. Mechanical strain has been identified as the proximal cause of axonal injury. Since the microstructure of the brain white matter is locally oriented, the stress and strain fields are highly axon orientation dependent. The accuracy of the finite element simulations depends not only on correct determination of the material properties but also on precise depiction of the tissues’ microstructure (microscopic level). We applied a finite element method and a mircomechanics approach to simulate the kinematics of axon, which was developed according to experimental data, and found that the degree of coupling between the axons and surrounding cells within the tissue will affect the behavior of the tissue. In this study, the finite element model and the kinematic axonal model are applied to the Representative Volume Element (RVE) of central nervous system (CNS) white matter to investigate the tissue level mechanical behavior. The uniaxial tensile test on the white matter tissue will be presented as an example using the RVE.
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Reports on the topic "Spinal cord Axons Oligodendroglia"

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Sriram, Subramaniam. MALDI/Mass Spectrometry of Normal Appearing and Dystrophic Axons in Spinal Cord of Multiple Sclerosis (MS). Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada582356.

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Sriram, Subramaniam. MALDI/Mass Spectrometry of Normal Appearing" and Dystrophic Axons in Spinal Cord of Multiple Sclerosis (MS)". Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada592436.

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