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Debroas, Guilhaume, Guillaume Hoeffel, Ana Reynders, and Sophie Ugolini. "Interactions neuro-immunes dans la peau." médecine/sciences 34, no. 5 (May 2018): 432–38. http://dx.doi.org/10.1051/medsci/20183405016.
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Lors d’une infection, notre capacité à éliminer les pathogènes dépend essentiellement de notre système immunitaire. Des études récentes révèlent cependant un rôle du système nerveux dans la régulation des processus infectieux et inflammatoires. Des interactions fonctionnelles bidirectionnelles s’établissent entre systèmes nerveux et immunitaire pour préserver l’intégrité des tissus. La peau constitue l’une des premières lignes de défense contre les menaces extérieures et présente un système neuro-immun particulièrement développé. En cas de lésion cutanée, des neurones impliqués dans la perception douloureuse sont activés et modulent la fonction et le recrutement des cellules immunitaires au sein du tissu. Nous illustrons ici l’importance de ces régulations neuro-immunes à travers différents exemples de pathologies cutanées.
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Bonnet, Nicolas, Daniel Courteix, and Claude Laurent Benhamou. "Leptine, système nerveux central et tissu osseux : influence de l'exercice physique." Revue du Rhumatisme 72, no. 10-11 (October 2005): 890–93. http://dx.doi.org/10.1016/j.rhum.2005.09.002.
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Moreau, Marc, Catherine Leclerc, and Isabelle Néant. "La saga de l’induction neurale : presque un siècle de recherche." médecine/sciences 36, no. 11 (November 2020): 1018–26. http://dx.doi.org/10.1051/medsci/2020172.
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La formation du système nerveux débute par l’induction neurale, un processus qui permet aux cellules de l’ectoderme (tissu cible) d’acquérir un destin neural en réponse à des signaux provenant du mésoderme dorsal (tissu inducteur). Ce processus, décrit en 1924 sur l’amphibien, n’a reçu une explication moléculaire qu’au milieu des années 1990. Pendant cette période, plusieurs auteurs se sont intéressés au rôle joué par la membrane du tissu cible mais peu de travaux décisifs ont décrit la transduction du signal neuralisant. Entre 1990 et 2019, nous avons disséqué la transduction du signal neuralisant, un sujet très peu abordé alors. Nous avons souligné le rôle nécessaire et suffisant du calcium pour orienter les cellules de l’ectoderme vers un destin neural et établi la cascade moléculaire allant de l’activation de canaux membranaires à la transcription de gènes.
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Levasseur, Régis, Jean-Pierre Sabatier, Céline Potrel-Burgot, Bertrand Lecoq, Christian Creveuil, and Christian Marcelli. "Le système nerveux sympathique est un médiateur des contraintes mécaniques dans le tissu osseux." Revue du Rhumatisme 70, no. 12 (December 2003): 1100–1104. http://dx.doi.org/10.1016/j.rhum.2003.07.004.
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Behar-Cohen, Francine, Emmanuelle Gelizé, Laurent Jonet, and Patricia Lassiaz. "Anatomie de la rétine." médecine/sciences 36, no. 6-7 (June 2020): 594–99. http://dx.doi.org/10.1051/medsci/2020094.
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La neurorétine est une unité fonctionnelle du système nerveux central assurant la conversion d’un signal lumineux en un influx nerveux. D’origine neuroectodermique, dérivée du diencéphale, la neurorétine est un tissu stratifié, composé de six types de cellules neuronales (deux types de photorécepteurs : les cônes et les bâtonnets ; les cellules horizontales, bipolaires, amacrines et ganglionnaires) et de trois types de cellules gliales (les cellules gliales de Müller, les astrocytes et les cellules microgliales). La neurorétine repose sur l’épithélium pigmentaire rétinien, l’ensemble constituant la rétine. L’existence des barrières hémato-rétiniennes interne et externe et des jonctions intra-rétiniennes rend compte de la finesse de la régulation des échanges de la rétine avec la circulation et au sein de la rétine elle-même. La zone centrale de la rétine humaine, la macula, zone hautement spécialisée pour assurer l’acuité visuelle, présente des spécificités anatomiques. Les méthodes d’imagerie récentes permettent d’enrichir nos connaissances sur les caractéristiques anatomiques et fonctionnelles de la rétine, qui restent encore imparfaitement décrites.
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Ballout, Nissrine, Sophie Péron, and Afsaneh Gaillard. "Restauration des voies corticales lésées par greffe de neurones." médecine/sciences 34, no. 8-9 (August 2018): 678–84. http://dx.doi.org/10.1051/medsci/20183408014.
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Le cortex moteur joue un rôle central dans le contrôle, la planification et l’exécution des commandes motrices volontaires chez les mammifères et la perte de neurones corticaux est une caractéristique commune à de nombreuses conditions neuropathologiques, comme les lésions traumatiques, ischémiques ou certaines maladies neurodégénératives. Afin de pallier les capacités limitées de régénération spontanée des neurones du système nerveux central adulte, des stratégies de remplacement cellulaire, par transplantation de tissu immature, présentent un potentiel prometteur. Dans cette revue, nous présenterons un rappel historique de la transplantation au niveau du cerveau et l’état actuel de la recherche dans le domaine de la transplantation corticale.
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LANTIER, F., D. MARC, P. SARRADIN, P. BERTHON, R. MERCEY, F. EYCHENNE, O. ANDREOLETTI, F. SCHELCHER, and J. M. ELSEN. "Le diagnostic des encéphalopathies spongiformes chez les ruminants." INRAE Productions Animales 17, HS (December 20, 2004): 79–85. http://dx.doi.org/10.20870/productions-animales.2004.17.hs.3632.
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Le diagnostic des Encéphalopathies Spongiformes Transmissibles (EST) des ruminants est aujourd’hui basé sur la mise en évidence de l’isoforme pathologique, résistante à la protéinase K, de la protéine PrP, la PrPres. La PrPres peut être mise en évidence in situ, à l’aide de techniques immunohistochimiques ou, bien après extraction et traitement à la protéinase K, par des techniques immunochimiques (western blot, Enzyme Linked ImmunoSorbent Assay). Si le diagnostic de routine des encéphalopathies spongiformes animales a fait de gros progrès ces dernières années, il demeure un diagnostic post-mortem qui n’est applicable qu’aux tissus nerveux d’animaux suffisamment âgés pour permettre la formation de dépôts de PrPres dans le système nerveux central. La biopsie d’amygdales offre une possibilité de diagnostic ante-mortem chez les seuls animaux dont le tissu lymphoïde présente une accumulation de PrPres, les ovins génétiquement sensibles et la chèvre. Deux voies de développement des tests sont poursuivies actuellement : d’une part la mise au point d’un diagnostic sanguin précoce basé sur la détection de PrPres ou d’un autre marqueur spécifique de l’incubation d’une EST, et d’autre part des tests permettant de distinguer entre elles les souches de prion, notamment la souche Encéphalopathie Spongiforme Bovine (ESB). Ces évolutions constitueraient un progrès considérable pour notre compréhension des modes de transmission des EST et pour l’efficacité de la prophylaxie sanitaire.
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CHEMINEAU, P., M. BLANC, A. CARATY, G. BRUNEAU, and P. MONGET. "Sous-nutrition, reproduction et système nerveux central chez les mammifères : rôle de la leptine." INRAE Productions Animales 12, no. 3 (June 1, 1999): 217–23. http://dx.doi.org/10.20870/productions-animales.1999.12.3.3881.
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La relation entre la quantité de réserves adipeuses et la reproduction est connue depuis longtemps, mais le moyen par lequel les animaux sont capables d’estimer leur propre contenu en lipides corporels n’est connu que depuis peu. La leptine, une hormone principalement synthétisée et sécrétée par le tissu adipeux, identifiée en 1994, joue en grande partie ce rôle. Cette hormone agit sur des récepteurs spécifiques, présents dans de nombreux tissus. Chez les rongeurs, la leptine est impliquée dans la régulation centrale de l’ingestion alimentaire, de l’équilibre énergétique, de la thermorégulation, de l’activité reproductrice ainsi que dans la régulation de l’angiogenèse et des processus de cicatrisation.
Pour la régulation de l’activité des neurones à LHRH (Luteinising Hormone-Releasing Hormone, le décapeptide hypothalamique qui contrôle la synthèse et la libération de LH et de FSH dans l’hypohyse), la leptine agit au niveau hypothalamique, sur la forme longue du récepteur. Son action, indirecte, passerait très probablement par des neuromédiateurs tels que le neuropeptide Y (NPY), la pro-opiomélanocortine (POMC), la sérotonine ou la galanine. Des récepteurs à la leptine se rencontrent également dans l’hypophyse, les gonades et le placenta. Chez les ruminants, la leptine et ses récepteurs n’ont été identifiés et clonés que récemment ; leurs rôles sont en cours de détermination.
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Vily-Petit, J., M. Soty, A. Gautier-Stein, F. Rajas, M. Silva, M. Micoud, and G. Mithieux. "La néoglucogenèse intestinale active la thermogenèse du tissu adipeux brun en mobilisant le système nerveux sympathique." Annales d'Endocrinologie 82, no. 5 (October 2021): 270. http://dx.doi.org/10.1016/j.ando.2021.08.046.
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Calcagnotto, G. N., and J. Braga Silva. "La réparation de pertes de substance des nerves digitaux avec la technique de la greffe veineuse plus interposition de tissu nerveux. Étude prospective et randomisée." Chirurgie de la Main 25, no. 3-4 (September 2006): 126–30. http://dx.doi.org/10.1016/j.main.2006.07.033.
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GATTI, J. L., J. L. VILOTTE, M. OLLIVIER-BOUSQUET, and M. ELOIT. "Recherche d’une rôle physiologique pour la protéine prion cellulaire (PrPc)." INRAE Productions Animales 17, HS (December 20, 2004): 55–60. http://dx.doi.org/10.20870/productions-animales.2004.17.hs.3628.
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De nombreuses études sont menées pour élucider le mécanisme de la transformation de la protéine prion normale (PrPc) en protéine pathogène résistante aux protéases (PrPres) et pour comprendre comment l’accumulation de cette PrPres peut induire les dégénérescences nerveuses observées lors des Encéphalopathies Spongiformes Transmissibles (EST). Cependant, la protéine prion est une protéine ubiquitaire présente dans de nombreux tissus autres que le tissu nerveux et le rôle cellulaire «normal» joué par cette PrPc est très controversé et reste encore une énigme. Différentes équipes INRA utilisent leurs compétences en physiologie pour établir la présence et les voies de sécrétions de la protéine prion normale dans différents organes. Ces études se font en utilisant des modèles animaux et cellulaires classiques, mais aussi des souris où le gène codant pour la protéine prion est supprimé (PrP-/-) ou sa quantité sur-exprimée par introduction de multiples copies de ce gène. Ceci permettra d’une part d’étudier le ou les rôles possibles de cette protéine dans les différents tissus et fluides biologiques (protection contre le stress oxydatif, transport de métaux, signalisation cellulaire, etc.), d’autre part de rechercher si lors de l’infection, de la protéine prion pathogène est retrouvée dans certains de ces fluides biologiques tels que le lait et le sperme. En effet, si les études passées n’ont jamais montré de protéine prion pathogène dans ces fluides, des travaux utilisant des méthodes plus sensibles sont nécessaires pour confirmer ces résultats.
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PICARD-HAGEN, N., V. GAYRARD, C. VIGUIE, V. LAROUTE, and P. ALAYRAC. "Absence d’efficacité de la quinacrine dans le traitement des maladies à prions : possible explication à caractère pharmacologique." INRAE Productions Animales 17, HS (June 8, 2020): 101–8. http://dx.doi.org/10.20870/productions-animales.2004.17.hs.3634.
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En raison des incertitudes épidémiologiques relatives aux maladies à prions, il est urgent de découvrir et de développer des thérapeutiques anti-prions chez l’homme. L’efficacité des molécules candidates est essentiellement testée in vitro sur des cellules de neuroblastome. Pour plusieurs molécules, dont la quinacrine, il a été observé une discordance entre l’effet anti-prion in vitro et l’absence d’efficacité clinique dans le traitement de la maladie de Creutzfeldt-Jakob. Pour documenter l’hypothèse selon laquelle l’absence d’efficacité de la quinacrine était d’ordre pharmacocinétique (et donc prévisible), la disposition de la quinacrine (disparition de la quinacrine du compartiment sanguin, qui résulte par exemple de processus de distribution et d’élimination du principe actif) a été étudiée à la fois in vivo et in vitro afin de déterminer les doses qu’il conviendrait d’administrer in vivo pour obtenir des concentrations efficaces dans la biophase. Le modèle de brebis naturellement atteintes de tremblante a été utilisé. Dans un premier temps, un essai thérapeutique contrôlé sur des brebis en phase clinique de tremblante a permis de confirmer ce qui était connu chez l’homme, c’est-à-dire l’absence d’efficacité clinique de la quinacrine. Sur le modèle in vitro reproduisant les conditions princeps de culture pour lesquelles 50 % de l’effet anti-prion avait été observé, avec une concentration nominale de quinacrine de 300 nM (nanomoles par litre), nous avons redéterminé les EC50 (concentration qui permet d’inhiber à 50 % la formation de PrP pathogène) pour les biophases potentielles de l’action anti-prion en mesurant sélectivement, par HPLC (chromatographie liquide haute performance), les véritables concentrations extracellulaire (120 nM) et intracellulaire (6700 nM) de quinacrine dans les neuroblastomes en culture. Les concentrations de quinacrine dans le Liquide Cérébro-Spinal (LCS) et le tissu nerveux cérébral, représentatifs in vivo respectivement des biophases extracellulaire et intracellulaire, ont été mesurées chez la brebis après une administration de quinacrine. Les concentrations de quinacrine dans le liquide cérébro-spinal (< 2,1 nM et 55 nM, obtenues respectivement pour des doses thérapeutique et toxique) sont restées très inférieures aux concentrations nécessaires pour obtenir in vitro un effet antiprion (120 nM). Les concentrations totales de quinacrine dans le tissu nerveux (1040 nM) après une dose thérapeutique sont restées inférieures aux concentrations de quinacrine actives in vitro (6700 nM) et, seule une dose toxique de quinacrine a permis d’atteindre des concentrations intracellulaires actives (53800 nM). En définitive, quelle que soit la biophase intra- ou extracellulaire, les schémas posologiques non toxiques sont incapables de maintenir des concentrations antiprion efficaces de quinacrine. A l’avenir, pour éviter des études in vivo dont on peut prévoir d’emblée qu’elles sont vouées à l’échec, notamment chez l’homme, il est recommandé de mesurer les EC50 anti-prions dans les biophases in vitro, pour évaluer si les effets anti-prion observés in vitro sont extrapolables in vivo.
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Ternier, Jessica. "Recherche de nouveaux marqueurs protéomiques par SELDI-TOF dans les tumeurs du système nerveux central : optimisation, « profiling » des épendymomes, étude préliminaire sur les appositions de tissu tumoral." Neurochirurgie 51, no. 6 (December 2005): 616. http://dx.doi.org/10.1016/s0028-3770(05)83648-3.
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SARRADIN, P., and H. LAUDE. "Diversité des souches d’Encéphalopathie Spongiforme Transmissible chez les ruminants : enjeux, bilan et perspectives." INRAE Productions Animales 17, HS (December 19, 2004): 13–20. http://dx.doi.org/10.20870/productions-animales.2004.17.hs.3617.
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Les Encéphalopathies Spongiformes Transmissibles (EST) ou maladies à prion se caractérisent par l’accumulation dans le tissu nerveux d’une forme anormalement repliée d’une protéine cellulaire de l’hôte, la PrPc. Cette isoforme anormale, ou PrPsc, supposée responsable des désordres neurodégénératifs observés, est aussi assimilée par de nombreux auteurs à l’agent transmissible lui-même, lequel serait alors dépourvu de génome et se propagerait de manière épigénétique. Un phénomène au coeur des recherches sur les EST est l’existence de variants phénotypiques, ou souches. Les souches de prions peuvent être différenciées entre elles sur une base biologique, par la nature des manifestations anatomo-pathologiques engendrées lors de leur propagation chez un même hôte, en particulier une lignée pure de souris, et sur une base biochimique, par le profil moléculaire de la PrPsc présente dans le cerveau des individus atteints. Le déterminisme biologique et moléculaire de cette diversité et la dynamique évolutive qu’elle suggère demeurent largement incompris. De ce fait, la caractérisation des souches qui infectent les espèces naturellement atteintes par les EST constitue une tâche relativement ardue, au demeurant essentielle à la compréhension de l’épidémiologie de ces maladies, à leur contrôle sur le terrain et à la protection de la santé humaine. Les recherches menées à l’INRA visent à documenter la diversité des souches d’EST chez les petits ruminants par typage des isolats de tremblante naturelle, et à mieux comprendre le déterminisme de cette diversité. Elles ont également pour objectif l’amélioration des méthodes actuelles de typage en termes de rapidité et de fiabilité, notamment à travers le développement de souris transgéniques plus réceptives à la transmission que les souris conventionnelles.
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Mwamengele, G. L. M., and S. Larsen. "L’ultrastructure de lamicrovasculature cérébrale de chèvres infectées expérimentalement avec Cowdria ruminantium." Revue d’élevage et de médecine vétérinaire des pays tropicaux 46, no. 1-2 (January 1, 1993): 245. http://dx.doi.org/10.19182/remvt.9372.
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Afin d’étudier les lésions de la microvasculature cérébrale dans la cowdriose, 14 chèvres tanzaniennes ont été infectées par inoculation intraveineuse avec le stock Ball-3 de Cowdria ruminantium. Elles ont été suivies sur le plan clinique pendant la période d’incubation et la réaction fébrile, et sacrifiées lorsque les températures ont commencé à baisser. Cinq chèvres saines ont été utilisées pour déterminer la meilleure procédure pour la fixation du cerveau par perfusion et pour servir de témoins. La perfusion a été effectuée par l’artère carotide sous anesthésie générale au pentobarbitone, utilisant du glutaraldehyde de pH 7,4 à 3 p.100, à 500 mOsm. Des prélèvements de tissu cérébral ont été pris pour microscopie classique et électronique. Des signes variables de désordres du système nerveux central et un hydropéricarde peu important se sont développés chez toutes les chèvres infectées. Deux changements neuropathologiques différents ont été observés : des colonies de Cowdria dans des cellules endothéliales vasculaires, sans autres changements, et des petites infiltrations périvasculaires de cellules mononucléaires. Aucun signe de vasculite ou d’une perméabilité vasculaire anormale n’a été observé. Plusieurs phagocytes périvasculaires renfermaient des inclusions cytoplasmiques inhabituelles, se présentant comme des agrégations de particules irrégulièrement arrondies, associées à une membrane, de 0,25 à 0,4 µm de diamètre, ayant dans quelques cas une structure interne évocatrice de mitochondries partiellement dégradées. Néanmoins, ces agrégations ne semblaient pas enfermées de façon convaincante à l’intérieur de membranes, comme il est à à prévoir en cas d’autophagocytose. Une autre interprétation hypothétique est qu’elles représentent des stades abortifs de C. ruminantium qui tentent de se développer en dehors des vaisseaux et qu’une réponse immunitaire cellulaire, développée pendant et après la période d’incubation, limite ce deuxième cycle dans l’hôte et provoque des infiltrations périvasculaires mononucléaires.
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Wang, Lei G., Connor W. Barth, Catherine H. Kitts, Mubark D. Mebrat, Antonio R. Montaño, Broderick J. House, Meaghan E. McCoy, et al. "Near-infrared nerve-binding fluorophores for buried nerve tissue imaging." Science Translational Medicine 12, no. 542 (May 6, 2020): eaay0712. http://dx.doi.org/10.1126/scitranslmed.aay0712.
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Nerve-binding fluorophores with near-infrared (NIR; 650 to 900 nm) emission could reduce iatrogenic nerve injury rates by providing surgeons precise, real-time visualization of the peripheral nervous system. Unfortunately, current systemically administered nerve contrast agents predominantly emit at visible wavelengths and show nonspecific uptake in surrounding tissues such as adipose, muscle, and facia, thus limiting detection to surgically exposed surface-level nerves. Here, a focused NIR fluorophore library was synthesized and screened through multi-tiered optical and pharmacological assays to identify nerve-binding fluorophore candidates for clinical translation. NIR nerve probes enabled micrometer-scale nerve visualization at the greatest reported tissue depths (~2 to 3 mm), a feat unachievable with previous visibly emissive contrast agents. Laparoscopic fluorescent surgical navigation delineated deep lumbar and iliac nerves in swine, most of which were invisible in conventional white-light endoscopy. Critically, NIR oxazines generated contrast against all key surgical tissue classes (muscle, adipose, vasculature, and fascia) with nerve signal-to-background ratios ranging from ~2 (2- to 3-mm depth) to 25 (exposed nerve). Clinical translation of NIR nerve-specific agents will substantially reduce comorbidities associated with surgical nerve damage.
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Giordano, Antonio, Andrea Frontini, Incoronata Murano, Cristina Tonello, M. Antonella Marino, Michele O. Carruba, Enzo Nisoli, and Saverio Cinti. "Regional-dependent Increase of Sympathetic Innervation in Rat White Adipose Tissue during Prolonged Fasting." Journal of Histochemistry & Cytochemistry 53, no. 6 (June 2005): 679–87. http://dx.doi.org/10.1369/jhc.4a6566.2005.
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White adipose tissue (WAT) is innervated by the sympathetic nervous system. A role for WAT sympathetic noradrenergic nerves in lipid mobilization has been suggested. To gain insight into the involvement of nerve activity in the delipidation process, WAT nerves were investigated in rat retroperitoneal and epididymal depots after prolonged fasting. A significant increase in tyrosine hydroxylase (TH) content was found in epididymal and, especially, retroperitoneal WAT by Western blotting. Accordingly, an increased immunoreactivity for TH was detected by immunohistochemistry in epididymal and, especially, retroperitoneal vascular and parenchymal noradrenergic nerves. Neuropeptide Y (NPY)-containing nerves were found around arteries and in the parenchyma. Double-staining experiments and confocal microscopy showed that most perivascular and some parenchymal noradrenergic nerves also contained NPY. Detection of protein gene product (PGP) 9.5, a general marker of peripheral nerves, by Western blotting and PGP 9.5-TH by double-staining experiments showed significantly increased noradrenergic nerve density in fasted retroperitoneal, but not epididymal depots, suggesting that formation of new nerves takes place in retroperitoneal WAT in fasting conditions. On the whole, these data confirm the important role of sympathetic noradrenergic nerves in WAT lipid mobilization during fasting but also raise questions about the physiological role of regional-dependent nerve adjustments and their functional significance in relation to white adipocyte secretory products.
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Zhang, Fengshi, Meng Zhang, Songyang Liu, Ci Li, Zhentao Ding, Teng Wan, and Peixun Zhang. "Application of Hybrid Electrically Conductive Hydrogels Promotes Peripheral Nerve Regeneration." Gels 8, no. 1 (January 6, 2022): 41. http://dx.doi.org/10.3390/gels8010041.
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Peripheral nerve injury (PNI) occurs frequently, and the prognosis is unsatisfactory. As the gold standard of treatment, autologous nerve grafting has several disadvantages, such as lack of donors and complications. The use of functional biomaterials to simulate the natural microenvironment of the nervous system and the combination of different biomaterials are considered to be encouraging alternative methods for effective tissue regeneration and functional restoration of injured nerves. Considering the inherent presence of an electric field in the nervous system, electrically conductive biomaterials have been used to promote nerve regeneration. Due to their singular physical properties, hydrogels can provide a three-dimensional hydrated network that can be integrated into diverse sizes and shapes and stimulate the natural functions of nerve tissue. Therefore, conductive hydrogels have become the most effective biological material to simulate human nervous tissue’s biological and electrical characteristics. The principal merits of conductive hydrogels include their physical properties and their electrical peculiarities sufficient to effectively transmit electrical signals to cells. This review summarizes the recent applications of conductive hydrogels to enhance peripheral nerve regeneration.
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Brown, Danielle L., Michael Staup, and Cynthia Swanson. "Stereology of the Peripheral Nervous System." Toxicologic Pathology 48, no. 1 (June 20, 2019): 37–48. http://dx.doi.org/10.1177/0192623319854746.
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Qualitative histopathology has been the gold standard for evaluation of morphological tissue changes in all organ systems, including the peripheral nervous system. However, the human eye is not sensitive enough to detect small changes in quantity or size. Peripheral nervous system toxicity can manifest as subtle changes in neuron size, neuron number, axon size, number of myelinated or unmyelinated axons, or number of nerve fibers. Detection of these changes may be beyond the sensitivity of the human eye alone, necessitating quantitative approaches in some cases. Although 2-dimensional (2D) histomorphometry can provide additional information and is more sensitive than qualitative evaluation alone, the results are not always representative of the entire tissue and assumptions about the tissue can lead to bias, or inaccuracies, in the data. Design-based stereology provides 3D estimates of number, volume, surface area, or length, and stereological principles can be applied to peripheral nervous system tissues to obtain accurate and precise estimates, such as neuron number and size, axon number, and total intraepidermal nerve fiber length. This review describes practical stereological approaches to 3 compartments of the peripheral nervous system: ganglia, peripheral nerves, and intraepidermal nerve fibers.
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Masters, Barry R., and Andreas A. Thaer. "Real-time scanning-slit in vivo confocal microscope based on bilateral scanning which solves the problem of specimen motion blur: Applications to ocular neuroimaging." Proceedings, annual meeting, Electron Microscopy Society of America 52 (1994): 228–29. http://dx.doi.org/10.1017/s0424820100168876.
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The standard method to observe nerves in tissue is to use some agent such as silver or gold compounds which are localized in the nerve fibers and increase their contrast. These were the techniques developed by Camillo Golgi and Santiago Ramón y Cajal. Cajal’s work was published in a two-volume edition in French in 1909 with the title Histologie du Systéme Nerveux de l’ Homme et des Vertébrés. This work was republished in 1952-1955 as Histologie du Systéme Nerveux by L. Azoulay, Instituto Ramón y Cajal.Alternatively a fluorescent compound may be introduced near the cell bodies of the neurons and the compound diffuses along the lipid membranes of the nerve. Subsequent observations of the specimen in a fluorescent microscope provides the observer with a bright, high contrast image of the nerve and its branches and bifurcations.The standard instrument for the observation of the cornea is the slit-lamp. The slit-lamp was invented by Allvar Gullstrand. Gullstrand made major contributions to the theory of astigmatism and to the mechanism of accommodation of the eye.
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Chi, E. Y., M. L. Su, Y. T. Tien, and W. R. Henderson. "Mast cell-nerve fiber interaction: Ultrastructural studies." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 428–29. http://dx.doi.org/10.1017/s0424820100159680.
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Recent attention has been directed to the interaction of the nerve and immune systems. The neuropeptide substance P, a tachykinnin which is a neurotransmitter in the central and peripheral nervous systems produces tissue swelling, augemntation of intersitial fibrin deposition and leukocyte infiltration after intracutaneous injection. There is a direct correlation reported between the extent of mast cell degranulation at the sites of injection and the tissue swelling or granulocyte infiltration. It has previously been demonstrated that antidromic electrical stimulation of sensory nerves induces degranulation of cutaneous mast cells, cutaneous vasodilation and augmented vascular permeability. Morphological studies have documented a close anatiomical association between mast cells and nonmyelinated nerves, that contain substance P and other neuropeptides. However, the presence of mast cells within nerve fasicles has not been previously examined ultrastructurally. In this study, we examined ultrastructurally the distribution of mast cells in the nerve fiber bundles located in the muscular connective tissue of rat tongues (n=20).
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Giannessi, Elisabetta, Maria Stornelli, Alessandra Coli, and Pier Sergi. "A Quantitative Investigation on the Peripheral Nerve Response within the Small Strain Range." Applied Sciences 9, no. 6 (March 16, 2019): 1115. http://dx.doi.org/10.3390/app9061115.
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Peripheral nerves are very complex biological structures crucial to linking the central nervous system to the periphery of the body. However, their real behaviour is partially unknown because of the intrinsic difficulty of studying these structures in vivo. As a consequence, theoretical and computational tools together with in vitro experiments are widely used to approximate the mechanical response of the peripheral nervous tissue to different kind of solicitations. More specifically, particular conditions narrow the mechanical response of peripheral nerves within the small strain regime. Therefore, in this work, the mechanical response of nerves was investigated through the study of the relationships among strain, stress and displacements within the small strain range. Theoretical predictions were quantitatively compared to experimental evidences, while the displacement field was studied for different values of the tissue compressibility. This framework provided a straightforward computational assessment of the nerve response, which was needed to design suitable connections to biomaterials or neural interfaces within the small strain range.
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Kolar, Mallappa K., and Paul J. Kingham. "Regenerative effects of adipose-tissue-derived stem cells for treatment of peripheral nerve injuries." Biochemical Society Transactions 42, no. 3 (May 22, 2014): 697–701. http://dx.doi.org/10.1042/bst20140004.
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Peripheral nerve injuries are a common occurrence affecting the nerves found outside the central nervous system. Complete nerve transections necessitate surgical re-anastomosis, and, in cases where there is a significant gap between the two ends of the injured nerve, bridging strategies are required to repair the defect. The current clinical gold standard is the nerve graft, but this has a number of limitations, including donor site morbidity. An active area of research is focused on developing other techniques to replace these grafts, by creating tubular nerve-guidance conduits from natural and synthetic materials, which are often supplemented with biological cues such as growth factors and regenerative cells. In the present short review, we focus on the use of adipose-tissue-derived stem cells and the possible mechanisms through which they may exert a positive influence on peripheral nerve regeneration, thereby enabling more effective nerve repair.
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Hara, M., M. Toyoda, M. Yaar, J. Bhawan, E. M. Avila, I. R. Penner, and B. A. Gilchrest. "Innervation of melanocytes in human skin." Journal of Experimental Medicine 184, no. 4 (October 1, 1996): 1385–95. http://dx.doi.org/10.1084/jem.184.4.1385.
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Communication between the nervous system and epidermal melanocytes has been suspected on the basis of their common embryologic origin and apparent parallel involvement in several disease processes, but never proven. In this study, confocal microscopic analysis of human skin sections stained with antibodies specific for melanocytes and nerve fibers showed intraepidermal nerve endings in contact with melanocytes. This intimate contact was confirmed by electron microscopy, which further demonstrated thickening of apposing plasma membranes between melanocytes and nerve fibers, similar to synaptic contacts seen in nervous tissue. Since many intraepidermal nerve fibers are afferent nerves that act in a "neurosecretory" fashion through their terminals, cultured human melanocytes were stimulated with calcitonin gene-related peptide (CGRP), substance P, or vasoactive intestinal peptide, neuropeptides known to be present in cutaneous nerves, to examine their possible functions in the epidermal melanin unit. CGRP increased DNA synthesis rate of melanocytes in a concentration- and time-dependent manner. Cell yields after 5 d were increased 25% compared with controls maintained in an otherwise optimized medium. Furthermore, stimulation by CGRP induced rapid and dose-dependent accumulation of intracellular cAMP, suggesting that the mitogenic effect is mediated by the cAMP pathway. These studies confirm and expand a single earlier report in an animal model of physical contact between melanocytes and cutaneous nerves and for the first time strongly suggest that the nervous system may exert a tonic effect on melanocytes in normal or diseased human skin.
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Němec, Ivo, Václav Smrčka, and Jaroslav Pokorný. "The Effect of Sensory Innervation on the Inorganic Component of Bones and Teeth; Experimental Denervation – Review." Prague Medical Report 119, no. 4 (2018): 137–47. http://dx.doi.org/10.14712/23362936.2019.1.
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The effect of the nervous system on bone remodelling has been described by many studies. Sensory and autonomic nerves are present in the bone. Immunohistochemical analysis of the bone have indicated the presence of neuropeptides and neurotransmitters that act on bone cells through receptors. Besides carrying sensory information, sensory neurons produce various neuropeptides playing an important role in maintaining bone and tooth pulp homeostasis, and dentin formation. Bone tissue and teeth contain organic and inorganic components. Bone cells enable bone mineralization and ensure its formation and resorption. Studies focused on the effects of the nervous system on the bone are proceeded using various ways. Sensory denervation itself can be achieved using capsaicin causing chemical lesion to the nerve. Surgical ways of causing only sensory lesion to nerves are substantially limited because many peripheral nerves are mixed and contain a motor component as well. From this point of view, the experimental model with transection of inferior alveolar nerve is appropriate. This nerve provides sensory innervation of the bone and teeth of the mandible. The purpose of our paper is to provide an overview of the effects exerted by the nervous system on the inorganic component of the bone and teeth, and also to present an overview of the used experimental models. As we assume, the transection of inferior alveolar nerve could be reflected in changed contents and distribution of chemical elements in the bone and teeth of rat mandible. This issue has not been studied so far.
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Egawa, M., H. Yoshimatsu, and G. A. Bray. "Effect of beta-endorphin on sympathetic nerve activity to interscapular brown adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 1 (January 1, 1993): R109—R115. http://dx.doi.org/10.1152/ajpregu.1993.264.1.r109.
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beta-Endorphin was injected into the third cerebroventricle to investigate its effects on sympathetic nerve activity to interscapular brown adipose tissue (IBAT) in rats. Multiunit discharges of sympathetic nerves to IBAT were recorded electrophysiologically in anesthetized rats. The intracerebroventricular injection of beta-endorphin (125, 250, and 500 pmol/rat in 10 microliters) suppressed sympathetic nerve activity in a dose-related fashion (-23.9 +/- 20.4, -38.7 +/- 7.1, and -66.7 +/- 7.6% 30 min after injection) compared with preinjection baseline. N-acetyl-beta-endorphin (250 pmol) had no effect on sympathetic nerve activity to IBAT. The intraperitoneal injection of naloxone (5.0 mg/rat) did not affect sympathetic nerve activity, but preinjection of naloxone inhibited the suppressive effect of intracerebroventricular injection of beta-endorphin (250 pmol). We conclude that the intracerebroventricular administration of beta-endorphin suppressed the sympathetic nerve activity to IBAT through opioid receptors. The results of this experiment are consistent with the hypothesis that beta-endorphin has a reciprocal effect on food intake and the sympathetic nervous system.
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Antunes-Duarte, Sofia, Pablo Espinosa Lara, Marta Aguado Lobo, Tiago Oliveira, Ana Fraga, Dolores López-Presa, Luís Soares-de-Almeida, and Paulo Filipe. "Cutaneous Ancient Schwannoma of the Ear." Journal of the Portuguese Society of Dermatology and Venereology 79, no. 2 (June 26, 2021): 169–71. http://dx.doi.org/10.29021/spdv.79.2.1312.
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Schwannoma is a benign encapsulated nerve sheath tumor composed of Schwann cells, that may arise anywhere along the course of a nerve. Cutaneous schwannomas, associated with peripheral nerves, usually present as a slow-growing well-circumscribed nodule, localized in the dermis or subcutaneous tissue. They are generally asymptomatic; however, they may become painful by the nervous compression. Since the clinical signs are non-specific, histology is required for a definitive diagnosis. Herein, we present a case of a solitary cutaneous ancient schwannoma of the ear, a histopathological variant of schwannoma with distinctive morphological characteristics.
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Ramazanov, G. R., E. V. Shevchenko, L. I. Idilova, V. N. Stepanov, E. V. Nugaeva, and S. S. Petrikov. "Neurosarcoidosis." Russian neurological journal 25, no. 5 (December 16, 2020): 45–50. http://dx.doi.org/10.30629/2658-7947-2020-25-5-45-50.
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The article represents the discussion of sarcoidosis involving the cranial nerves and meninges. It’s a rare disease difficult to diagnose. This form of the disease is a progressive lesion of the nervous system, characterized by granulomatous inflammation of the membranes and /or tissue of cerebrum or spinal cord, cranial and /or peripheral nerves. Clinical signs of the nervous system disorder found in sarcoidosis, are detected only in 5–15% of patients. They are often represented by symptoms of cranial nerve damage, meningeal syndrome and epileptic seizures. X-ray computed tomography and magnetic resonance imaging of the brain do not reveal specific changes, however, they allow to exclude other structural lesions of the central nervous system and to identify neuroimaging signs, most common in the course of this disease. Diagnosis of neurosarcoidosis is possible in the presence of neurological symptoms, signs of multisystem lesions, and histological confirmation of non-caseous granulomatous inflammation in one or more organs. The article also represents a clinical observation of a patient with neurosarcoidosis, manifested by acute bilateral neuropathy of the facial nerves, unilateral neuropathy of the trigeminal nerve and meningism syndrome. The neuroimaging signs, often found in this disease, were revealed: the accumulation of contrast agent by the membranes of the brain and the tissue of cavum Meckeli. The course of the disease and diagnostic search, which made it possible to detect signs of multisystem lesion, are described. The diagnosis was confirmed by histological examination of the biopsy material of the intrathoracic lymph node. The results of neurosarcoidosis anti-inflammatory therapy are presented. The peculiarities influencing the choice of this type of treatment terms, are indicated.
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Giordano, Antonio, C. Kay Song, Robert R. Bowers, J. Christopher Ehlen, Andrea Frontini, Saverio Cinti, and Timothy J. Bartness. "White adipose tissue lacks significant vagal innervation and immunohistochemical evidence of parasympathetic innervation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (November 2006): R1243—R1255. http://dx.doi.org/10.1152/ajpregu.00679.2005.
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Converging evidence indicates that white adipose tissue (WAT) is innervated by the sympathetic nervous system (SNS) based on immunohistochemical labeling of a SNS marker (tyrosine hydroxylase [TH]), tract tracing of WAT sympathetic postganglionic innervation, pseudorabies virus (PRV) transneuronal labeling of WAT SNS outflow neurons, and functional evidence from denervation studies. Recently, WAT para-SNS (PSNS) innervation was suggested because local surgical WAT sympathectomy (sparing hypothesized parasympathetic innervation) followed by PRV injection yielded infected cells in the vagal dorsomotor nucleus (DMV), a traditionally-recognized PSNS brain stem site. In addition, local surgical PSNS WAT denervation triggered WAT catabolic responses. We tested histologically whether WAT was parasympathetically innervated by searching for PSNS markers in rat, and normal (C57BL) and obese ( ob/ob) mouse WAT. Vesicular acetylcholine transporter, vasoactive intestinal peptide and neuronal nitric oxide synthase immunoreactivities were absent in WAT pads (retroperitoneal, epididymal, inguinal subcutaneous) from all animals. Nearly all nerves innervating WAT vasculature and parenchyma that were labeled with protein gene product 9.5 (PGP9.5; pan-nerve marker) also contained TH, attesting to pervasive SNS innervation. When Siberian hamster inguinal WAT was sympathetically denervated via local injections of catecholaminergic toxin 6-hydroxydopamine (sparing putative parasympathetic nerves), subsequent PRV injection resulted in no central nervous system (CNS) or sympathetic chain infections suggesting no PSNS innervation. By contrast, vehicle-injected WAT subsequently inoculated with PRV had typical CNS/sympathetic chain viral infection patterns. Collectively, these data indicate no parasympathetic nerve markers in WAT of several species, with sparse DMV innervation and question the claim of PSNS WAT innervation as well as its functional significance.
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Egawa, M., H. Yoshimatsu, and G. A. Bray. "Neuropeptide Y suppresses sympathetic activity to interscapular brown adipose tissue in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 2 (February 1, 1991): R328—R334. http://dx.doi.org/10.1152/ajpregu.1991.260.2.r328.
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To investigate the effects of neuropeptide Y (NPY) on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), we injected NPY into the third cerebroventricle (icv), medial preoptic area (MPOA), anterior hypothalamic area (AHA), paraventricular hypothalamic nucleus (PVN), ventromedial hypothalamic nucleus (VMN), and lateral hypothalamic area (LHA) of anesthetized rats. Multiunit discharges from sympathetic nerves to IBAT were recorded electrophysiologically. The icv injection of NPY suppressed sympathetic nerve activity in a dose-dependent manner, followed by a gradual recovery. The microinjection of NPY (25 pmol) unilaterally into the PVN also significantly suppressed the sympathetic nerve activity to IBAT. In contrast, microinjection of NPY into the MPOA significantly increased the sympathetic nerve activity. The injection of saline into either the PVN or MPOA had no significant effect on sympathetic nerve activity. The microinjection of NPY (25 pmol) into the AHA, VMN, or LHA did not change sympathetic nerve activity to IBAT. We conclude that central administration of NPY affects the sympathetic nerve activity to IBAT and that the suppressive effect of NPY, which may act in part through the PVN, is dominant to the stimulatory effect. The result is consistent with the hypothesis that NPY is a neurochemical modulator of the sympathetic nervous system which controls energy expenditure in IBAT.
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HUANG, YI-CHENG, and YI-YOU HUANG. "TISSUE ENGINEERING FOR NERVE REPAIR." Biomedical Engineering: Applications, Basis and Communications 18, no. 03 (June 25, 2006): 100–110. http://dx.doi.org/10.4015/s101623720600018x.
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Nerve regeneration is a complex biological phenomenon. Once the nervous system is impaired, its recovery is difficult and malfunctions in other parts of the body may occur because mature neurons don't undergo cell division. To increase the prospects of axonal regeneration and functional recovery, researches have focused on designing “nerve guidance channels” or “nerve conduits”. For developing tissue engineered nerve conduits, four components come to mind, including a scaffold for axonal proliferation, supporting cells such as Schwann cells, growth factors, and extracelluar matrix. This article reviews the nervous system physiology, the factors that are critical for nerve repair, and the advanced technologies that are explored to fabricate nerve conduits. Furthermore, we also introduce a new method we developed to create longitudinally oriented channels within biodegradable polymers, Chitosan and PLGA, using a combined lyophilizing and wire-heating process. This innovative method using Ni-Cr wires as mandrels to create nerve guidance channels. The process is easy, straightforward, highly reproducible, and could easily be tailored to other polymer and solvent systems. These scaffolds could be useful for guided regeneration after transection injury in either the peripheral nerve or spinal cord.
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Bizzozero, Laura, Margherita Pergolizzi, Davide Pascal, Elena Maldi, Giulia Villari, Jessica Erriquez, Marco Volante, et al. "Tumoral Neuroligin 1 Promotes Cancer–Nerve Interactions and Synergizes with the Glial Cell Line-Derived Neurotrophic Factor." Cells 11, no. 2 (January 14, 2022): 280. http://dx.doi.org/10.3390/cells11020280.
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Many nervous proteins are expressed in cancer cells. In this report, we asked whether the synaptic protein neuroligin 1 (NLGN1) was expressed by prostatic and pancreatic carcinomas; in addition, given the tendency of these tumors to interact with nerves, we asked whether NLGN1 played a role in this process. Through immunohistochemistry on human tissue microarrays, we showed that NLGN1 is expressed by prostatic and pancreatic cancer tissues in discrete stages and tumor districts. Next, we performed in vitro and in vivo assays, demonstrating that NLGN1 promotes cancer cell invasion and migration along nerves. Because of the established role of the neurotrophic factor glial cell line-derived neurotrophic factor (GDNF) in tumor–nerve interactions, we assessed a potential NLGN1–GDNF cooperation. We found that blocking GDNF activity with a specific antibody completely inhibited NLGN1-induced in vitro cancer cell invasion of nerves. Finally, we demonstrated that, in the presence of NLGN1, GDNF markedly activates cofilin, a cytoskeletal regulatory protein, altering filopodia dynamics. In conclusion, our data further prove the existence of a molecular and functional cross-talk between the nervous system and cancer cells. NLGN1 was shown here to function along one of the most represented neurotrophic factors in the nerve microenvironment, possibly opening new therapeutic avenues.
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Kaplan, Ben, and Shulamit Levenberg. "The Role of Biomaterials in Peripheral Nerve and Spinal Cord Injury: A Review." International Journal of Molecular Sciences 23, no. 3 (January 23, 2022): 1244. http://dx.doi.org/10.3390/ijms23031244.
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Peripheral nerve and spinal cord injuries are potentially devastating traumatic conditions with major consequences for patients’ lives. Severe cases of these conditions are currently incurable. In both the peripheral nerves and the spinal cord, disruption and degeneration of axons is the main cause of neurological deficits. Biomaterials offer experimental solutions to improve these conditions. They can be engineered as scaffolds that mimic the nerve tissue extracellular matrix and, upon implantation, encourage axonal regeneration. Furthermore, biomaterial scaffolds can be designed to deliver therapeutic agents to the lesion site. This article presents the principles and recent advances in the use of biomaterials for axonal regeneration and nervous system repair.
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Grisold, Wolfgang, and Anna Grisold. "Cancer around the brain." Neuro-Oncology Practice 1, no. 1 (March 1, 2014): 13–21. http://dx.doi.org/10.1093/nop/npt002.
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Abstract Background Neuro-oncologists are familiar with primary brain tumors, intracerebral metastases meningeal carcinomatosis and extracerebral intracranial tumors as meningeoma. For these conditions, and also some other rare tumor entities several treatment options exist. Cancer can also involve structures around the brain as the dura, the base of the skull, the cavities of the skull and tissue around the bony skull, the skin, the tissue of the neck. and either compress, invade or spread in the central or peripheral nervous system. Methods A systematic literature research was conducted determining symptoms and signs, tumor sites of nerve invasion, tumor types, diagnostic techniques, mechanisms of nerve invasion, and important differential diagnosis. Additional cases from own experience were added for illustration. Results The mechanisms of tumor invasion of cranial nerves is heterogenous and not only involves several types of invasion, but also spread along the cranial nerves in antero- and retrograde fashion and even spread into different nerve territories via anastomosis. In addition the concept of angiosomas may have an influence on the spread of metastases. Conclusion In addition to the well described tumor spread in meningeal carcinomatosis and base of the skull metastases, dural spread, lesions of the bony skull, the cavities of the skull and skin of the face and tissue of the neck region need to be considered, and have an impact on therapeutic decisions.
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Baraldi, James H., German V. Martyn, Galina V. Shurin, and Michael R. Shurin. "Tumor Innervation: History, Methodologies, and Significance." Cancers 14, no. 8 (April 14, 2022): 1979. http://dx.doi.org/10.3390/cancers14081979.
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The role of the nervous system in cancer development and progression has been under experimental and clinical investigation since nineteenth-century observations in solid tumor anatomy and histology. For the first half of the twentieth century, methodological limitations and opaque mechanistic concepts resulted in ambiguous evidence of tumor innervation. Differential spatial distribution of viable or disintegrated nerve tissue colocalized with neoplastic tissue led investigators to conclude that solid tumors either are or are not innervated. Subsequent work in electrophysiology, immunohistochemistry, pathway enrichment analysis, neuroimmunology, and neuroimmunooncology have bolstered the conclusion that solid tumors are innervated. Regulatory mechanisms for cancer-related neurogenesis, as well as specific operational definitions of perineural invasion and axonogenesis, have helped to explain the consensus observation of nerves at the periphery of the tumor signifying a functional role of nerves, neurons, neurites, and glia in tumor development.
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Bartness, Timothy J., C. Kay Song, Haifei Shi, Robert R. Bowers, and Michelle T. Foster. "Brain–adipose tissue cross talk." Proceedings of the Nutrition Society 64, no. 1 (February 2005): 53–64. http://dx.doi.org/10.1079/pns2004409.
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While investigating the reversible seasonal obesity of Siberian hamsters, direct sympathetic nervous system (SNS) postganglionic innervation of white adipose tissue (WAT) has been demonstrated using anterograde and retrograde tract tracers. The primary function of this innervation is lipid mobilization. The brain SNS outflow to WAT has been defined using the pseudorabies virus (PRV), a retrograde transneuronal tract tracer. These PRV-labelled SNS outflow neurons are extensively co-localized with melanocortin-4 receptor mRNA, which, combined with functional data, suggests their involvement in lipolysis. The SNS innervation of WAT also regulates fat cell number, as noradrenaline inhibits and WAT denervation stimulates fat cell proliferation in vitro and in vivo respectively. The sensory innervation of WAT has been demonstrated by retrograde tract tracing, electrophysiological recording and labelling of the sensory-associated neuropeptide calcitonin gene-related peptide in WAT. Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by non-excised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey information about body fat levels to the brain. Finally, parasympathetic nervous system innervation of WAT has been suggested, but the recent finding of no WAT immunoreactivity for the possible parasympathetic marker vesicular acetylcholine transporter (VAChT) argues against this claim. Collectively, these data suggest several roles for efferent and afferent neural innervation of WAT in body fat regulation.
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Sheikh, S. P., J. J. Holst, T. Skak-Nielsen, U. Knigge, J. Warberg, E. Theodorsson-Norheim, T. Hokfelt, J. M. Lundberg, and T. W. Schwartz. "Release of NPY in pig pancreas: dual parasympathetic and sympathetic regulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 1 (July 1, 1988): G46—G54. http://dx.doi.org/10.1152/ajpgi.1988.255.1.g46.
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Several lines of evidence have connected neuropeptide Y (NPY), a 36-residue polypeptide, to the sympathetic division of the autonomic nervous system. We studied the localization, the molecular characteristics, and the release of NPY and norepinephrine (NE) in the porcine pancreas. Immunohistochemical investigations revealed that NPY nerves around blood vessels were likely to be of adrenergic nature, whereas NPY-immunoreactive fibers close to exocrine and endocrine cells may originate from local ganglia also containing VIP (vasoactive intestinal peptide) and PHI (peptide histidine isoleucine). Electrical stimulation of the splanchnic nerve supply to the isolated perfused pig pancreas resulted in a corelease of NPY and NE into the venous effluent. Stimulation of the vagal nerves caused a sevenfold larger release of NPY without affecting the NE secretion. Characterization of the NPY immunoreactivity in the pancreatic tissue and in the venous effluent by gel filtration, high-performance liquid chromatography, and isoelectric focusing showed that the immunoreactive NPY was indistinguishable from synthetic porcine NPY. It is concluded that, although NPY is associated with sympathetic perivascular neurons, the majority of the pancreatic NPY-containing nerve fibers are likely to belong to the parasympathetic division of the autonomic nervous system.
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Maiuolo, Jessica, Micaela Gliozzi, Vincenzo Musolino, Cristina Carresi, Saverio Nucera, Roberta Macrì, Miriam Scicchitano, et al. "The Role of Endothelial Dysfunction in Peripheral Blood Nerve Barrier: Molecular Mechanisms and Pathophysiological Implications." International Journal of Molecular Sciences 20, no. 12 (June 20, 2019): 3022. http://dx.doi.org/10.3390/ijms20123022.
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The exchange of solutes between the blood and the nerve tissue is mediated by specific and high selective barriers in order to ensure the integrity of the different compartments of the nervous system. At peripheral level, this function is maintained by the Blood Nerve Barrier (BNB) that, in the presence, of specific stressor stimuli can be damaged causing the onset of neurodegenerative processes. An essential component of BNB is represented by the endothelial cells surrounding the sub-structures of peripheral nerves and increasing evidence suggests that endothelial dysfunction can be considered a leading cause of the nerve degeneration. The purpose of this review is to highlight the main mechanisms involved in the impairment of endothelial cells in specific diseases associated with peripheral nerve damage, such as diabetic neuropathy, erectile dysfunction and inflammation of the sciatic nerve.
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Adakal, O., SI Mounkeila, O. Kimso, MB Abdoulaye, AN Hamma, M. Maikassoua, and MM Rouga. "C87: Les tumeurs des parties molles en service de chirurgie du Centre Hospitalier Régional de Maradi (Niger) en 2020." African Journal of Oncology 2, no. 1 Supplement (March 1, 2022): S36—S37. http://dx.doi.org/10.54266/ajo.2.1s.c87.blww8757.
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INTRODUCTION : Les tumeurs des parties molles sont définies comme des tumeurs développées au dépend des tissus non-épithéliaux de l’organisme, à l'exclusion des viscères, du tissu lymphoïde et du système nerveux central. On distingue les tumeurs bénignes qui sont de loin les plus fréquentes. Leur diagnostic est suspecté par le clinicien et confirmé par l’histo-pathologiste. Les tumeurs malignes sont beaucoup plus rares. (1% des cancers de l'adulte). Elles posent, du fait de leur rareté, de leur diversité histologique et de leur hétérogénéité évolutive, des problèmes diagnostic clinique, anatomopathologique, et thérapeutique. La prise en charge de ces tumeurs ne peut se concevoir en dehors de comités de concertation pluridisciplinaire associant chirurgiens, radiologues, anatomo-pathologistes, oncologues et radiothérapeutes. Notre étude se fixe comme objectif de déterminer les aspects épidémiologiques et thérapeutiques des tumeurs des parties molles au CHR de Maradi. MATERIELS ET METHODES : Nous rapportons 116 cas de tumeur des parties molles recensés du 1er Janvier au 31 Décembre 2020. L’âge moyen de nos patients était de 48 ans avec des extrêmes de 16 et 72 ans. Une prédominance masculine (sex-ratio=1,58). Le délai moyen de consultation était de 28 mois. Le siège de la tumeur était : les membres (82%), le tronc (6%), la tête et cou (12%). Les signes cliniques étaient dominés par une tuméfaction des parties molles (97%). Les tumeurs bénignes représentaient 65% alors que les tumeurs malignes représentaient 35%. Les Tumeurs bénignes étaient dominées par les lipomes (82%) les tumeurs musculaires représentaient 12%. Quant aux tumeurs malignes, les sarcomes représentaient 52% et les mélanomes 38%. La chirurgie était réalisée chez 71% des patients, elle était palliative chez 53% des cas et seulement 10% des patients opérée ont bénéficié d’un curage. La chimiothérapie y était associée en cas d’indication, elle était adjuvante dans 60% des cas. La radiothérapie a été réalisée chez 5% des patients (hors du pays), Les patients perdus de vue étaient de 58%. Une rechute locale a été observée dans 71%. Une rémission complète a marqué l’évolution de 17% des cas. Des métastases à distance ont retrouvé dans 48% des cas, la survie à trois mois était de 75% et à neuf mois 53%. Les défis étaient : une consultation tardive, un nombre important de patients perdus de vue, une chirurgie incomplète car parfois non indiquée et nous déplorons la faible réalisation d’examens complémentaires indispensables au diagnostic, à la stadification et à l’élaboration d’une stratégie thérapeutique adaptée. L’ouverture de l’unité de radiothérapie à Niamey sera l’occasion de définir la place de chacun des trois volets thérapeutiques : chirurgie, chimiothérapie et radiothérapie dans le processus thérapeutique de ces tumeurs, à travers l’élaboration de protocoles standardisés de traitement. Tout ceci ne fait que souligner l’intérêt primordial de la concertation multidisciplinaire dans la prise en charge des tumeurs malignes des parties molles. Ainsi que la nécessité de créer un groupe de travail et de recherche dédié à ces tumeurs. CONCLUSION : Les tumeurs des parties molles constituent un spectre large, hétérogène et complexe. Elles sont dominées par les tumeurs bénignes mais leur incidence réelle reste à déterminée. Leur diagnostic est clinique et histopathologique. Cette étude nous a aider à dresser un certain profil de ces tumeurs même si une étude de plus grande envergure s’impose. Les tumeurs malignes des parties molles posent très souvent des problèmes diagnostiques (anatomopathologique), d’évaluation pronostique et de stratégie thérapeutique. En effet, des études plus approfondies et concentrées sur la pathologie tumorale maligne des parties molles indépendamment de la pathologie tumorale bénigne sont impératives.
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Giangrande, A., M. A. Murray, and J. Palka. "Development and organization of glial cells in the peripheral nervous system of Drosophila melanogaster." Development 117, no. 3 (March 1, 1993): 895–904. http://dx.doi.org/10.1242/dev.117.3.895.
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We have used enhancer trap lines as markers to recognize glial cells in the wing peripheral nervous system of Drosophila melanogaster. Their characterization has enabled us to define certain features of glial differentiation and organization. In order to ask whether glial cells originate within the disc or whether they migrate to the wing nerves from the central nervous system, we used two approaches. In cultured wing discs from glial-specific lines, peripheral glial precursors are already present within the imaginal tissue during the third larval stage. Glial cells differentiate on a wing nerve even in mutants in which that nerve does not connect to the central nervous system. To assess whether peripheral glial cells originate from ectoderm or from mesoderm, we cultured discs from which the mesodermally derived adepithelial cells had been removed. Our findings indicate that peripheral glial cells originate from ectodermally derived cells. As has already been shown for the embryonic central nervous system, gliogenesis in the periphery is an early event during adult development: glial cells, or their precursors, are already present at stages when neurons are still differentiating. Finally, our results also suggest that peripheral glial cells may not display a stereotyped arrangement.
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Kakita, Yutaka, Kiyohiko Oshiro, D. Sean O'Briain, and Prem Puri. "Selective Demonstration of Mural Nerves in Ganglionic and Aganglionic Colon by Immunohistochemistry for Glucose Transporter-1." Archives of Pathology & Laboratory Medicine 124, no. 9 (September 1, 2000): 1314–19. http://dx.doi.org/10.5858/2000-124-1314-sdomni.
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Abstract Objective.—Hypertrophic nerves have long been considered a histopathologic feature of the aganglionic segment in Hirschsprung disease, but they remain incompletely explained. The purpose of this study was to define the nature and diagnostic importance of hypertrophic nerves in Hirschsprung disease and to clarify their relation to nearby smaller nerve fibers. Methods.—We used an immunoperoxidase staining technique to compare the distribution of 2 nerve markers—erythrocyte-type glucose transporter (GLUT-1), a marker of perineurium, and nerve growth factor receptor, a marker of both nerve fibers and perineurium—in aganglionic tissue (12 resected specimens and 4 rectal biopsies) and control tissue (6 autopsy specimens and 17 rectal biopsies) of children. Results.—In control ganglionic tissue, the myenteric and submucosal areas contained only occasional GLUT-1–positive nerves (usually less than 50 μm in diameter), but extramural extrinsic (serosal) nerves were invariably positive for GLUT-1. In aganglionic tissue, GLUT-1–positive nerves in the myenteric and submucosal areas were frequent and included both large (50–150 μm) and small (<50 μm) diameter nerves. Nerve growth factor receptor–positive fibers were frequent in all layers of all tissue studied. In aganglionic bowel, a distinct perineurium could be identified in the largest nerves, but nerve growth factor receptor had poor discrimination for small perineurium-sheathed nerves. Conclusion.—Most nerves, of both large and small diameter, in the myenteric and submucosal plexus of aganglionic bowel are GLUT-1 positive. Serosal extrinsic nerves stain identically, supporting the interpretation that the mural nerves are of extrinsic origin. Mural GLUT-1–positive nerves, when they are multiple and especially when they are greater than 50 μm in diameter (a figure which may be used as a threshold for hypertrophic nerves), are suggestive of Hirschsprung disease.
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Salomon, Benoît, Lesley Rhee, Helene Bour-Jordan, Honor Hsin, Anthony Montag, Betty Soliven, Jennifer Arcella, Ann M. Girvin, Stephen D. Miller, and Jeffrey A. Bluestone. "Development of Spontaneous Autoimmune Peripheral Polyneuropathy in B7-2–Deficient Nod Mice." Journal of Experimental Medicine 194, no. 5 (September 3, 2001): 677–84. http://dx.doi.org/10.1084/jem.194.5.677.
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An increasing number of studies have documented the central role of T cell costimulation in autoimmunity. Here we show that the autoimmune diabetes-prone nonobese diabetic (NOD) mouse strain, deficient in B7-2 costimulation, is protected from diabetes but develops a spontaneous autoimmune peripheral polyneuropathy. All the female and one third of the male mice exhibited limb paralysis with histologic and electrophysiologic evidence of severe demyelination in the peripheral nerves beginning at 20 wk of age. No central nervous system lesions were apparent. The peripheral nerve tissue was infiltrated with dendritic cells, CD4+, and CD8+ T cells. Finally, CD4+ T cells isolated from affected animals induced the disease in NOD.SCID mice. Thus, the B7-2–deficient NOD mouse constitutes the first model of a spontaneous autoimmune disease of the peripheral nervous system, which has many similarities to the human disease, chronic inflammatory demyelinating polyneuropathy (CIDP). This model demonstrates that NOD mice have “cryptic” autoimmune defects that can polarize toward the nervous tissue after the selective disruption of CD28/B7-2 costimulatory pathway.
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Otagiri, Risa, Hideki Kawai, Masanobu Takatsuka, Naoki Shinyashiki, Akira Ito, Ryosuke Ikeguchi, and Tomoki Aoyama. "Interfacial polarization of in vivo rat sciatic nerve with crush injury studied via broadband dielectric spectroscopy." PLOS ONE 16, no. 6 (June 2, 2021): e0252589. http://dx.doi.org/10.1371/journal.pone.0252589.
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Electrical stimulation is one of the candidates for elongation-driven regeneration of damaged peripheral nerves. Different organs and tissues have an inherent cell structure and size. This leads to variation in the tissue-specific electrical properties of the frequency of interfacial polarization. Although nervous tissues have a membrane potential, the electrical reaction inside these tissues following electrical stimulation from outside remains unexplored. Furthermore, the pathophysiological reaction of an injured nerve is unclear. Here, we investigated the electrical reaction of injured and non-injured rat sciatic nerves via broadband dielectric spectroscopy. Crush injured and non-injured sciatic nerves of six 12-week-old male Lewis rats were used, 6 days after infliction of the injury. Both sides of the nerves (with and without injury) were exposed, and impedance measurements were performed at room temperature (approximately 25°C) at frequencies ranging from 100 mHz to 5.5 MHz and electric potential ranging from 0.100 to 1.00 V. The measured interfacial polarization potentially originated from the polarization by ion transport around nerve membranes at frequencies between 3.2 kHz and 1.6 MHz. The polarization strength of the injured nerves was smaller than that of non-injured nerves. However, the difference in polarization between injured and non-injured nerves might be caused by inflammation and edema. The suitable frequency range of the interfacial polarization can be expected to be critical for electrical stimulation of injured peripheral nerves.
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MacEwan, Matthew R., Paul Gamble, Manu Stephen, and Wilson Z. Ray. "Therapeutic electrical stimulation of injured peripheral nerve tissue using implantable thin-film wireless nerve stimulators." Journal of Neurosurgery 130, no. 2 (February 2019): 486–95. http://dx.doi.org/10.3171/2017.8.jns163020.
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OBJECTIVEElectrical stimulation of peripheral nerve tissue has been shown to accelerate axonal regeneration. Yet existing methods of applying electrical stimulation to injured peripheral nerves have presented significant barriers to clinical translation. In this study, the authors examined the use of a novel implantable wireless nerve stimulator capable of simultaneously delivering therapeutic electrical stimulation of injured peripheral nerve tissue and providing postoperative serial assessment of functional recovery.METHODSFlexible wireless stimulators were fabricated and implanted into Lewis rats. Thin-film implants were used to deliver brief electrical stimulation (1 hour, 20 Hz) to sciatic nerves after nerve crush or nerve transection-and-repair injuries.RESULTSElectrical stimulation of injured nerves via implanted wireless stimulators significantly improved functional recovery. Brief electrical stimulation was observed to increase the rate of functional recovery after both nerve crush and nerve transection-and-repair injuries. Wireless stimulators successfully facilitated therapeutic stimulation of peripheral nerve tissue and serial assessment of nerve recovery.CONCLUSIONSImplantable wireless stimulators can deliver therapeutic electrical stimulation to injured peripheral nerve tissue. Implantable wireless nerve stimulators might represent a novel means of facilitating therapeutic electrical stimulation in both intraoperative and postoperative settings.
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Miroshnikova, Polina K., Alexey V. Lyundup, Nikolay P. Batsalenko, Mikhail E. Krasheninnikov, Yuanyuan Zhang, Natalia B. Feldman, and Valeriy V. Beregovykh. "Perspective Nerve Conduits for Stimulation of Regeneration of Damaged Peripheral Nerves." Annals of the Russian academy of medical sciences 73, no. 6 (December 12, 2018): 388–400. http://dx.doi.org/10.15690/vramn1063.
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Nerve damage is a common severe trauma caused by a complete or partial disruption of the integrity of the nerve trunk and appropriate dissociation of the CNS and denervated tissue. «Golden standard» in the treatment of extensive injuries of peripheral nerves is the use of autografts of nerve fibers, but when they are used, pathological disturbances appear in the donor zone and the results of surgical treatment are not always satisfactory. Currently, an alternative to the traditional method is the use of nerve conduits (conductors) for directed regeneration of axons. In this work, the results of the application of nerve conductors from various materials and with various biologically active components in preclinical and clinical studies, as well as conduits used in clinical practice, were analyzed. The efficiency of regeneration was compared, on the basis of the analysis the conductor most suitable for successful nerve regeneration was selected, including approaches for creating innervated tissue engineered constructs. In this work, we have collected research on nerve conductors from various materials with various prescribed properties using certain factors used to treat damage to the peripheral nervous system, showing all the advantages and disadvantages of their use, which makes it possible to develop and create a conduit that meets all the requirements of modern regenerative medicine.
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Diez-Ahedo, Ruth, Xabier Mendibil, Mari Carmen Márquez-Posadas, Iban Quintana, Francisco González, Francisco Javier Rodríguez, Leyla Zilic, et al. "UV-Casting on Methacrylated PCL for the Production of a Peripheral Nerve Implant Containing an Array of Porous Aligned Microchannels." Polymers 12, no. 4 (April 22, 2020): 971. http://dx.doi.org/10.3390/polym12040971.
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Peripheral nerves are basic communication structures guiding motor and sensory information from the central nervous system to receptor units. Severed peripheral nerve injuries represent a large clinical problem with relevant challenges to successful synthetic nerve repair scaffolds as substitutes to autologous nerve grafting. Numerous studies reported the use of hollow tubes made of synthetic polymers sutured between severed nerve stumps to promote nerve regeneration while providing protection for external factors, such as scar tissue formation and inflammation. Few approaches have described the potential use of a lumen structure comprised of microchannels or microfibers to provide axon growth avoiding misdirection and fostering proper healing. Here, we report the use of a 3D porous microchannel-based structure made of a photocurable methacrylated polycaprolactone, whose mechanical properties are comparable to native nerves. The neuro-regenerative properties of the polymer were assessed in vitro, prior to the implantation of the 3D porous structure, in a 6-mm rat sciatic nerve gap injury. The manufactured implants were biocompatible and able to be resorbed by the host’s body at a suitable rate, allowing the complete healing of the nerve. The innovative design of the highly porous structure with the axon guiding microchannels, along with the observation of myelinated axons and Schwann cells in the in vivo tests, led to a significant progress towards the standardized use of synthetic 3D multichannel-based structures in peripheral nerve surgery.
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Fortin, Jessica S., Elizabeth A. Chlipala, Daniel P. Shaw, and Brad Bolon. "Methods Optimization for Routine Sciatic Nerve Processing in General Toxicity Studies." Toxicologic Pathology 48, no. 1 (May 22, 2019): 19–29. http://dx.doi.org/10.1177/0192623319850774.
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Recent “best practice” recommendations for peripheral nervous system sampling and processing provide guidance regarding nerve preparation for animal toxicity studies. This study explored the impact of delayed fixation, type of fixative, processing cycle times, starting ethanol concentration, and water bath temperature to improve nerve preservation in routinely prepared (paraffin-embedded, hematoxylin and eosin [H&E]-stained) sections. Sciatic nerves from adult Wistar rats (diameter, 1.04 ± 0.1 mm) and young domestic pigs (diameter 5.9 ± 1.2 mm) fixed at necropsy (“0” hours) or 3, 6, 12, or 24 hours after death were immersed in neutral-buffered 10% formalin containing 1.2% methanol (NBF) or methanol-free 4% formaldehyde (MFF) at room temperature. After fixation for 24 hours (rat) or 48 hours (pig), specimens were processed into paraffin, and ∼5-μm-thick sections were flattened on water baths set at 35°C, 40°C, or 45°C before H&E staining. Large-diameter nerves (pig) required longer processing cycles to ensure sufficient paraffin infiltration. For both small-diameter (rat) and large-diameter nerves, structural integrity was optimal if fixation by NBF or MFF occurred within 3 hours and the initial ethanol concentration for tissue processing was lowered to 50%. At all time points, structural preservation of nerve fibers was acceptable using NBF but was better with MFF. Use of a water bath at 35°C reduced processing-related nerve fiber separation within sections.
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Pjevic, Miroslava, Erzebet Patarica-Huber, Dragana Radovanovic, and Sanja Vickovic. "Neuropathic pain due to malignancy: Mechanisms, clinical manifestations and therapy." Medical review 57, no. 1-2 (2004): 33–40. http://dx.doi.org/10.2298/mpns0402033p.
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Introduction Neuropathic pain in cancer patients requires a focused clinical evaluation based on knowledge of common neuropathic pain syndromes. Definition Neuropathic pain is a non-nociceptive pain or "differentiation" pain, which suggests abnormal production of impulses by neural tissue that is separated from afferent input. Impulses arise from the peripheral nervous system or central nervous system. Causes of neuropathic pain due to malignancy Neuropathic pain is caused directly by cancer-related pathology (compression/infiltration of nerve tissue, combination of compression/infiltration) or by diagnostic and therapeutic procedures (surgical procedures, chemotherapy, radiotherapy). Mechanisms Pathophysiological mechanisms are very complex and still not clear enough. Neuropathic pain is generated by electrical hyperactivity of neurons along the pain pathways. Peripheral mechanisms (primary sensitization of nerve endings, ectopically generated action potentials within damaged nerves, abnormal electrogenesis within sensory ganglia) and central mechanisms (loss of input from peripheral nociceptors into dorsal horn, aberrant sprouting within dorsal horn, central sensitization, loss of inhibitory interneurons, mechanisms at higher centers) are involved. Diagnosis The quality of pain presents as spontaneous pain (continuous and paroxysmal), abnormal pain (allodynia, hyperalgesia, hyperpathia), paroxysmal pain. Clinical manifestations Clinically, neuropathic pain is described as the pain in the peripheral nerve (cranial nerves, other mononeuropathies, radiculopathy, plexopathy, paraneoplastic peripheral neuropathy) and relatively infrequent, central pain syndrome. Therapy Treatment of neuropathic pain remains a challenge for clinicians, because there is no accepted algorithm for analgesic treatment of neuropathic pain. Pharmacotherapy is considered to be the first line therapy. Opioids combined with non-steroidal antiinflammatory drugs are warrented. If patient is relatively unresponsive to an opioid, a trial with adjuvant analgesics might be considered. Tricyclic antidepressants might be selected for patients with continuous dysesthesia, and anticonvulsants might be used if the pain is predominanty lancinating or paroxysmal. The complexity of neuropathic syndromes and underlying etiologic mechanisms warrant clinical trials to determine appropriate treatment.
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Lytvyn, K. Yu, L. R. Shostakovych-Koretska, Z. O. Chykarenko, O. A. Kushnierova, I. V. Budaeva, and O. O. Bilokon. "CLINICAL PARALLELS IN INFECTIOUS DISEASES OF THE CENTRAL NERVOUS SYSTEM IN PATIENTS WITH HIV." International Medical Journal, no. 1 (March 5, 2020): 83–87. http://dx.doi.org/10.37436/2308-5274-2020-1-18.
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A retrospective analysis of medical records of 451 patients with HIV infection showed that the most common clinical manifestations of cerebral tuberculosis are as follows: headache, fever ≥ 38.0 °C, meningeal symptoms; in toxoplasmosis encephalitis these are headache, paresis of cranial nerves and extremities, incoordination, cognitive disorders, dysarthria, fever ≥ 38.0 °C and convulsions; in mycotic lesions of the CNS they are headache, coordination disorders, positive meningeal symptoms, disturbances of consciousness, cognitive disorders, visual disorders, cranial nerve deficiency, convulsions and dysarthria. The clinical picture of bacterial (exacted) meningitis was dominated by positive meningeal symptoms, headache, fever, impaired consciousness. At the same time, in such neurological manifestations of central nervous system lesions as cranial nerve paresis, mono− and hemiparesis, visual, coordination and speech disorders, which mostly accompany cerebral toxoplasmosis, cerebrovascular diseases, brain tumors, encephalitis of unspecified etiology. Thus, the analysis suggests that the clinical manifestations of various etiologies of lesions of the central nervous system are often nonspecific and probably are stipulated with common morphological changes in brain tissue, which may be associated with the neuropathological effects of HIV, as well as a large impact co−infection. Key words: HIV infection, opportunistic infections, central nervous system, main symptoms.
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Leskovar, A., L. J. Moriarty, J. J. Turek, I. A. Schoenlein, and R. B. Borgens. "The macrophage in acute neural injury: changes in cell numbers over time and levels of cytokine production in mammalian central and peripheral nervous systems." Journal of Experimental Biology 203, no. 12 (June 15, 2000): 1783–95. http://dx.doi.org/10.1242/jeb.203.12.1783.
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We evaluated the timing and density of ED-1-positive macrophage accumulation (ED 1 is the primary antibody for the macrophage) and measured cytokine production by macrophages in standardized compression injuries to the spinal cord and sciatic nerves of individual rats 3, 5, 10 and 21 days post-injury. The actual site of mechanical damage to the nervous tissue, and a more distant site where Wallerian degeneration had occurred, were evaluated in both the peripheral nervous system (PNS) and the central nervous system (CNS) at these time points. The initial accumulation of activated macrophages was similar at both the central and peripheral sites of damage. Subsequently, macrophage densities at all locations studied were statistically significantly higher in the spinal cord than in the sciatic nerve at every time point but one. The peak concentrations of three cytokines, tumor necrosis factor α (TNF α), interleukin-1 (IL-1) and interleukin-6 (IL-6), appeared earlier and were statistically significantly higher in injured spinal cord than in injured sciatic nerve. We discuss the meaning of these data relative to the known differences in the reparative responses of the PNS and CNS to injury.