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Academic literature on the topic '110902 Cellular Nervous System'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "110902 Cellular Nervous System"

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Díaz-Balzac, Carlos A., Lionel D. Vázquez-Figueroa, and José E. García-Arrarás. "Novel markers identify nervous system components of the holothurian nervous system." Invertebrate Neuroscience 14, no. 2 (April 17, 2014): 113–25. http://dx.doi.org/10.1007/s10158-014-0169-1.

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Dockray, Graham. "The enteric nervous system." Neurochemistry International 12, no. 1 (January 1988): 103. http://dx.doi.org/10.1016/0197-0186(88)90156-8.

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Leonard, B. E. "The Cellular Structure of the Mammalian Nervous System." Neurochemistry International 11, no. 2 (January 1987): 249–50. http://dx.doi.org/10.1016/0197-0186(87)90020-9.

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Philbert, M. A., D. K. Waters, and H. E. Lowndes. "Cellular distribution of glutathione in the nervous system." Free Radical Biology and Medicine 9 (January 1990): 20. http://dx.doi.org/10.1016/0891-5849(90)90239-f.

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Brown, MarvinR, Jean Rivier, and Laurel Fisher. "Bombesin: Central nervous system actions to affect the autonomic nervous system." Regulatory Peptides 19, no. 1-2 (October 1987): 102. http://dx.doi.org/10.1016/0167-0115(87)90082-6.

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Flachenecker, Peter, and Karlheinz Reiners. "Autonomic nervous system testing." Muscle & Nerve 21, no. 5 (May 1998): 680. http://dx.doi.org/10.1002/(sici)1097-4598(199805)21:5<680::aid-mus25>3.0.co;2-y.

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Chen, H. S. "Immune Response in the Nervous System." Journal of Chemical Neuroanatomy 25, no. 4 (July 2003): 311. http://dx.doi.org/10.1016/s0891-0618(03)00020-6.

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Barnard, Eric A., Joseph Simon, and Tania E. Webb. "Nucleotide receptors in the nervous system." Molecular Neurobiology 15, no. 2 (October 1997): 103–29. http://dx.doi.org/10.1007/bf02740631.

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Yepes, Manuel. "TWEAK and the Central Nervous System." Molecular Neurobiology 35, no. 3 (August 1, 2007): 255–65. http://dx.doi.org/10.1007/s12035-007-0024-z.

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Breakefield, Xandra O., and Alfred I. Geller. "Gene transfer into the nervous system." Molecular Neurobiology 1, no. 4 (December 1987): 339–71. http://dx.doi.org/10.1007/bf02935741.

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Dissertations / Theses on the topic "110902 Cellular Nervous System"

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Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.

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Roshan, Payam. "Cellular basis of inflammation in the enteric nervous system." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26759.

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There is limited knowledge of immunocyte-myenteric neuronal interaction and the role of iNOS in myenteric neuronal injury. This research sought to examine the role of macrophages, NO, and iNOS inhibitors in myenteric neurodegeneration. Increased NO synthesis in macrophages and its effects on myenteric neurons were investigated in cell cultures. Using rodent models of inflammation, we further examined NO-dependent neurotoxicity. In the presence of activated macrophages neuronal injury and degeneration occurred; however the myenteric neurons showed greater resistance to oxidative challenge than cortical neurons. Pretreatment with iNOS inhibitors significantly reduced these inflammatory effects. Myenteric neuronal injury was also evident in experimental colitis, and iNOS selective inhibitor protected the myenteric neurons from inflammation and degeneration. In conclusion, these results show that activated macrophage-derived NO is important in inflammation-dependent myenteric neurodegeneration, and iNOS inhibitors can protect myenteric neurons from degeneration. Two potential strategies for neuroprotection in gut inflammation are defined.
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Ford, Melanie. "Cellular prion protein expression in the mouse." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249698.

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Balaskas, Christos. "Cellular development of the enteric nervous system in the chick embryo." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267801.

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Bogni, Silvia. "Molecular and cellular analysis of the enteric nervous system in vivo." Thesis, Open University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402166.

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Schuldt, Alison Jean. "The generation of cellular diversity in the Drosophila central nervous system." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624291.

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WILLIAMS, JON. "EFFECTS OF LOSS OF NF1 GENE ON PERIPHERAL NERVOUS SYSTEM PROGENITORS AND TUMORIGENESIS." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1212181112.

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Pliego-Rivero, Francisco Bernardo. "Thy-1 : cellular compartmentalization during development and participation in signal transduction." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358073.

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Franceschini, Isabelle A. "Cellular and molecular studies on olfactory bulb ensheathing cells." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301803.

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Brownlee, David Joseph Acheson. "Putative neurotransmitters in selected helminth parasites : cellular and subcellular localisation." Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296822.

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Books on the topic "110902 Cellular Nervous System"

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J, Siegel George, ed. Basic neurochemistry: Molecular, cellular, and medical aspects. 4th ed. New York: Raven Press, 1989.

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J, Siegel George, ed. Basic neurochemistry: Molecular, cellular, and medical aspects. 7th ed. Amsterdam: Elsevier, 2006.

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J, Siegel George, ed. Basic neurochemistry: Molecular, cellular, and medical aspects. 6th ed. Philadelphia: Lippincott Williams & Wilkins, 1998.

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Basic neurochemistry: Principles of molecular, cellular, and medical neurobiology. 8th ed. Amsterdam: Elsevier/Academic Press, 2012.

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Hillman, Harold. The Cellular Structure of the Mammalian Nervous System. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4922-5.

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Anacleto, Paços, and Nogueira Silvio, eds. Neurochemistry: Molecular aspects, cellular aspects, and clinical applications. Hauppauge, NY: Nova Science, 2009.

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A, Ribeiro J., ed. Adenosine receptors in the nervous system. London: Taylor & Francis, 1989.

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Schettler, Gotthard, Heiner Greten, and Andreas J. R. Habenicht, eds. Cellular Metabolism of the Arterial Wall and Central Nervous System. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84949-7.

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Schwann cells : development and regeneration of the nervous system. Brno: Masaryk University Brno, Medical Faculty, 1998.

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Haberman, Allan B. Cellular and tissue engineering. Waltham, Mass: Decision Resources, Inc., 1996.

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Book chapters on the topic "110902 Cellular Nervous System"

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Stone, T. W., and H. A. Simmonds. "Nervous system — cellular aspects." In Purines: Basic and Clinical Aspects, 90–114. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3911-3_6.

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Blaustein, M. P. "Cellular Calcium: Nervous System." In Calcium in Human Biology, 339–66. London: Springer London, 1988. http://dx.doi.org/10.1007/978-1-4471-1437-6_13.

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Fu, Xiaobing, Andong Zhao, and Tian Hu. "Central Nervous System and Dedifferentiation." In Cellular Dedifferentiation and Regenerative Medicine, 1–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-56179-9_1.

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Phillis, J. W. "Central Nervous System Effects of Adenosine." In Purines in Cellular Signaling, 41–47. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_6.

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Kilimann, Manfred W. "Protein Phosphorylation in the Nervous System." In Cellular Regulation by Protein Phosphorylation, 389–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75142-4_48.

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Steward, Oswald. "Histogenesis of the Nervous System." In Principles of Cellular, Molecular, and Developmental Neuroscience, 122–56. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3540-8_5.

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Matthews, Gary G. "Cardiac Muscle: The Autonomic Nervous System." In Cellular Physiology of Nerve and Muscle, 188–207. Malden, MA USA: Blackwell Publishing Ltd., 2013. http://dx.doi.org/10.1002/9781118687864.ch12.

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Huddie, P. L., D. L. Alkon, and D. S. Lester. "Cellular memory in an invertebrate." In Development and Regeneration of the Nervous System, 215–35. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2348-8_13.

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Hillman, Harold. "Cellular Identification — General Comments." In The Cellular Structure of the Mammalian Nervous System, 49–81. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4922-5_6.

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Matthews, Gary G. "Synaptic Transmission in the Central Nervous System." In Cellular Physiology of Nerve and Muscle, 130–59. Malden, MA USA: Blackwell Publishing Ltd., 2013. http://dx.doi.org/10.1002/9781118687864.ch9.

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Conference papers on the topic "110902 Cellular Nervous System"

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Barminko, Jeffrey, Jean Pierre Dolle, Rene Schloss, Martin Grumet, and Martin L. Yarmush. "Encapsulated Mesenchymal Stem Cells for Central Nervous System Repair." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19712.

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Mesenchymal stromal cells (MSC) have long been regarded as a cell source with the potential to provide therapies for various different tissue pathologies. They were originally identified for their ability to adhere to tissue culture plastic and gained favor due to their tremendous ability to propagate[1]. It was this finding as well as their ability to differentiate into lineages of mesoderm which have long made MSC a potential tool for autologous cellular replacement therapies [2, 3]. More recently, their cyto-protective role has been realized and been implicated in the benefit achieved in treating various different tissue pathologies. MSC have been found to secrete several different cytokines and growth factors in vitro. Furthermore, these factors can be modulated based on the environment MSC are exposed to. MSC have shown therapeutic benefits in models of GVHD, myocardial infarction, fulminant hepatic failure, central nervous system trauma and others, without any apparent cellular replacement. These advances propelled MSC to the fore front of potential cellular therapies and many are seeking to take advantage of their tissue protective properties. However, several draw backs in current methods of MSC implantation limit the ability to carry out safe and controlled clinical trials. Limitation with current MSC implantation approaches include; 1) directly transplanted MSCs exposed to the complex injury environment may be affected themselves early in the treatment processes, 2) MSC may also migrate to undesired tissue locations and 3) may differentiate into undesired end stage cells. These issues severally limit the translatability of MSC treatments in clinical settings; they make controlling experiments very difficult. There becomes a need to develop engineered methods for delivering these cells in a controlled manner. In order to circumvent these potential problems, we propose to use an alginate microencapsulation system as a vehicle for MSC delivery taking advantage of the soluble factors MSC provide.
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Mori, Yuki, Yasunobu Arima, Ting Chen, Dasong Zhu, Yutaka Komai, Masaaki Murakami, Yoshichika Yoshioka, Tetsuya Fujisawa, Syoji Kobashi, and Yutaka Hata. "In vivo MRI monitoring of inflammatory alterations and cellular dynamics in the central nervous system." In 2014 World Automation Congress (WAC). IEEE, 2014. http://dx.doi.org/10.1109/wac.2014.6935939.

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Belaya, О. V. "EXPERIMENTAL STUDY OF 2-5G BASE STATION ELECTROMAGNETIC FIELD CHRONIC EXPOSURE NERVOUS SYSTEM EFFECT TYPOLOGICAL FEATURES." In The 4th «OCCUPATION and HEALTH» International Youth Forum (OHIYF-2022). FSBSI «IRIOH», 2022. http://dx.doi.org/10.31089/978-5-6042929-6-9-2022-1-20-24.

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Introduction: the new exposure to electromagnetic fields biological effect assessment is actual with respect to the expected of electromagnetic environment complication due to joint operation of various generation cellular communication systems. The character of biological reaction can be mediated by individual typological characteristics of the organism. The goal: to study the 2–5G base stations electromagnetic field chronic exposure effect to nervous system functional state of laboratory animals with regard to their typological features. Methods: the rats body weight registration and "open field" test were carried out before the start of exposure, after each month of 24-hour exposure (500 µW/cm2, 2-5G mobile standards, 4 months) and 1 month after the end of exposure with accounting of high-entropic and low-entropic animal subgroups. Results: the results indicate a multidirectional effect of rats’ nervous system in groups of various entropy types. According to behavioral parameters and body weight dynamics, there was an inhibition of research activity and functional state of the high-entropic animals after 2 months of exposure. Conclusion: Results can be assumed that used experimental exposure type had a suppression affect to central nervous system functional state with higher responsiveness of animals that initially have a predominance of excitation over inhibition processes.
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Belov, Oleg, Ksenia Belokopytova, and Ara Bazyan. "ON MOLECULAR AND CELLULAR MECHANISMS OF RADIATION-INDUCED DISORDERS IN THE CENTRAL NERVOUS SYSTEM: STATUS OF RESEARCH AND PROSPECTS FOR DEVELOPMENT OF COUNTERMEASURES." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m943.sudak.ns2020-16/91-92.

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Smith, Katisha D., and Liang Zhu. "In Vivo Experimental Study of Rat Brain and Spinal Temperatures During Non-Invasive Spinal Cord Hypothermia Using a Cooling Pad." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53129.

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Traumatic injury causes mechanical tissue disruption that immediately follows a traumatic event. After the initial event, secondary injury often occurs. It is a cellular and molecular response to external trauma, including ischemia, inflammation, apoptosis, necrosis, and edema in the central nervous system (CNS). Since secondary injuries can lead to paralysis and permanent neurological damage, most current treatment are devoted to delaying or preventing secondary neurological injury.
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Jiang, Frank X., Penelope Georges, Uday Chippada, Lulu Li, Bernard Yurke, Rene S. Schloss, Bonnie L. Firestein, and Noshir A. Langrana. "Spinal Cord Neuronal Cell Properties Respond Differentially to the Stiffness of DNA Crosslinked Hydrogels." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192402.

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Mechanical cues arising from extracellular matrices greatly affect cellular properties, and hence, are of significance in designing biomaterials. Similar to many other cell types, including fibroblasts and hepatocytes, central nervous system (CNS) neurons have been found to exhibit distinct responses to the stiffness of the substrates they reside on [1]. There is an increasing awareness that mechanical properties also play a key role in successful utilization of scaffolds for those tissues whose major functions are not load-bearing, such as the spinal cord. In light of this, there is a growing interest in incorporating mechanical cues in biomaterial design for neural tissue engineering applications, including spinal cord injury.
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Castro, Ana Flávia Silva, Natália Barros Salgado Vieira, and Sarah Joanny da Silva Pereira. "Correlation between Zika virus and microcephaly as a consequence of congenital infection." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.629.

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Introduction: The Zika virus (ZIKV) is an arbovirus of RNA, whose transmission is mainly vector - by mosquitoes of the genus Aedes - but it also occurs through sexual, blood and transplacental transmission, with the last mentioned it was possible to verify serious neurological effects in the epidemic in South America, especially in Brazil, between 2015 and 2016. Objectives: To analyze the relationship between Zika virus infection and microcephaly in recent scientific literature. Methodology: Refers to a bibliographic review in the databases SciELO, LILACS and MEDLINE / Pubmed, with the terms “zika virus”, “infection” and “microcephaly” correlated in Portuguese and in English; 78 articles were found, but only 7 followed for analysis. Articles published more than 5 years ago and out of the proposed theme were disregarded. Results: The Zika virus, although similar to the dengue and chikungunya virus, it has a tendency to cause damage to the central nervous system such as Guillain-Barré Syndrome. However, the association between microcephaly and ZIKV started to be more observed through the increase of the disease among fetuses and newborns of mothers who had been infected during the gestational phase in the epidemic that happened in Brazil. It is known that the development of the nervous system is the product of processes of high proliferation and cellular differentiation, in which even small errors generate dangerous impacts, and it is during this period that ZIKV affects the CNS of the fetus. The disease is characterized by the reduction of the brain perimeter, in this context, is a consequence of abnormalities influenced by the virus. Conclusions: Microcephaly is a complex disease; therefore, it is necessary to emphasize the importance of primary care and other spheres for monitoring Zika virus infections, prenatal care and constant psychosocial monitoring. Furthermore, it is necessary to understand the relevance of studies about ZIKV and microcephaly, and to encourage scientific production in this area.
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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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Pasupathy, Parameshwaran, Robert De Simone, and Assimina A. Pelegri. "Numerical Simulation of Stress States in White Matter via a Continuum Model of 3D Axons Tethered to Glia." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-24667.

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Abstract A new finite element approach is proposed to study the propagation of stress in axons in the central nervous system (CNS) white matter. The axons are embedded in an extra cellular matrix (ECM) and are subjected to tensile loads under purely non-affine kinematic boundary conditions. The axons and the ECM are described by the Ogden hyperelastic material model. The effect of tethering of the axons by oligodendrocytes is investigated using the finite element model. Glial cells are often thought of as the “glue” that hold the axons together. More specifically, oligodendrocytes bond multiple axons to each other and create a myelin sheath that insulates and supports axons in the brainstem. The glial cells create a scaffold that supports the axons and can potentially bind 80 axons to a single oligodendrocyte. In this study, the microstructure of the oligodendrocyte connections to axons is modeled using a spring-dashpot approximation. The model allows for the oligodendrocytes to wrap around the outer diameter of the axons at various locations, parameterizing the number of connections, distance between connection points, and the stiffness of the connection hubs. The parameterization followed the distribution of axon-oligodendrocyte connections provided by literature data in which the values were acquired through microtome of CNS white matter. We develop two models: 1) multiple oligodendrocytes arbitrarily tethered to the nearest axons, and 2) a single oligodendrocyte tethered to all the axons at various locations. The results depict stiffening of the axons, which indicates that the oligodendrocytes do aid in the redistribution of stress. We also observe the appearance of bending stresses at inflections points along the tortuous path of the axons when subjected to tensile loading. The bending stresses appear to exhibit a cyclic variation along the length of the undulated axons. This makes the axons more susceptible to damage accumulation and fatigue. Finally, the effect of multiple axon-myelin connections in the central nervous system and the effect of the distribution of these connections in the brain tissue is further investigated at present.
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Nawroth, Peter P., Jerry Brett, Susan Steinberg, Charles T. Esmon, and David M. Stern. "ENDOTHELIUM AND PROTEIN S: SYNTHESIS, RELEASE AND REGULATION OF ANTICOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642962.

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The protein C-protein S pathway is closely linked to the vessel wall. In terms of protein C, endothelium has been shown to provide the receptor thrombomodulin, which promotes thrombin-mediated formation of activated protein C. Optimal anticoagulant function of activated protein C requires protein S and a cellular surface. Recent studies have indicated that endothelium can facilitate assembly of the activated protein C-protein S complex and that bovine endothelium expresses specific binding site(s) for protein S which promote its anticoagulant function. Expression of protein S binding sites is subject to down-regulation by Tumor Necrosis Factor (TNF) . Exposure of cultured bovine endothelium to TNF results in decreased 125I-protein s binding and attenuated rates of Factor Va inactivation after 2 hrs followed by negligible 125I-protein S binding and Factor Va inactivation by 10 hrs. These changes persist for over 48 hrs, in contrast to the more transient rise in endothelial cell tissue factor induced by TNF which returns to baseline by 24 hrs.In addition to providing binding sites for protein S, endothelium constitutively synthesizes and releases this vitamin K-dependent anticoagulant cofactor. Release of protein S is blocked by addition of warfarin, indicating that y-carboxylation facilitates the release of intracellular protein S. Morphologic studies, at the level of electron microscope, have shown protein S antigen to be present in cisternae of rough endoplasmic reticulum, the trans face of the golgi and a population of intracellular vesicles which appear to be distributed at the cellular periphery. By immunofluorescence, the distribution of protein S is distinct from that of von Willebrand Factor. The intracellular vesicles containing protein S constitute a storage pool potentially available for rapid release. Treatment of endothelium with norepinephrine results in release of protein S over the next 20 min. Release is half-maximal at a norepinephrine concentration of about 0.1 uM and is not observed with the biologically inactive entantiomer (+) norepinephrine. Norepinephrine-induced release of intracellular protein S can be blocked by prazosine (10-7 7 M), but not by propranolol (10-6 M) or yohimbine (10-5 M). These data are consistent with release of protein S being a receptor-mediated process dependent on an endothelial cell alpha 1 adrenergic receptor. Blockade of norepinephrine-induced release of protein S by pertussis toxin treatment of endothelium further defines the intracellular pathway of protein S and implicates regulatory G proteins in the stimulus-response coupling. Electron microscopic studies have shown that following exposure of endothelium to norepinephrine the intracellular vesicles containing protein S undergo exocytosis at the plasma membrane. These data define a new relationship between the autonomic nervous system and the coagulation mechanism.Protein S is clearly an endothelial cell-associated anticoagulant protein. A specific binding site on the endothelial cell surface can regulate its anticoagulant function on the vessel wall. Endothelial cell synthesis and release of protein S defines a new level of participation of endothelium in the protein C-protein S pathway.
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Reports on the topic "110902 Cellular Nervous System"

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Morphett, Jane, Alexandra Whittaker, Amy Reichelt, and Mark Hutchinson. Perineuronal net structure as a non-cellular mechanism of affective state, a scoping review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0075.

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Is the perineuronal net structure within emotional processing brain regions associated with changes in affective state? The objective of this scoping review is to bring together the literature on human and animal studies which have measured perineuronal net structure in brain regions associated with emotional processing (such as but not limited to amygdala, hippocampus and prefrontal cortex). Perineuronal nets are a specialised form of condensed extracellular matrix that enwrap and protect neurons (Suttkus et al., 2016), regulate synaptic plasticity (Celio and Blumcke, 1994) and ion homeostasis (Morawski et al., 2015). Perineuronal nets are dynamic structures that are influenced by external and internal environmental shifts – for example, increasing in intensity and number in response to stressors (Blanco and Conant, 2021) and pharmacological agents (Riga et al., 2017). This review’s objective is to generate a compilation of existing knowledge regarding the structural changes of perineuronal nets in experimental studies that manipulate affective state, including those that alter environmental stressors. The outcomes will inform future research directions by elucidating non-cellular central nervous system mechanisms that underpin positive and negative emotional states. These methods may also be targets for manipulation to manage conditions of depression or promote wellbeing. Population: human and animal Condition: affective state as determined through validated behavioural assessment methods or established biomarkers. This includes both positive and negative affective states. Context: PNN structure, measuringPNNs.
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