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Artículos de revistas sobre el tema "Transport neuronal":
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Sammler, Esther, Stefan Titz y Sheriar Hormuzdi. "Neuronal chloride transport tuning". Lancet 385 (febrero de 2015): S85. http://dx.doi.org/10.1016/s0140-6736(15)60400-7.
JODAL, M. "Neuronal influence on intestinal transport". Journal of Internal Medicine 228, S732 (noviembre de 1990): 125–32. http://dx.doi.org/10.1111/j.1365-2796.1990.tb01484.x.
Benaïssa, Ibtissem. "Analogie du transport neuronal au transport électronique en nanotechnologie". Journal of Renewable Energies 12, n.º 1 (26 de octubre de 2023): 9–28. http://dx.doi.org/10.54966/jreen.v12i1.115.
Le système nerveux est formé de deux types de cellules: les cellules gliales et les neurones. Les astrocytes, comme la plupart des cellules gliales, ont longtemps été considérés essentiellement pour leur rôle de support et d’entretien du tissu nerveux. Mais, de plus en plus d’évidences plaident en faveur d’une implication beaucoup plus importante des astrocytes dans la communication nerveuse. Les astrocytes sont couplés les uns aux autres par des ‘gap-jonctions’ à travers lesquels peuvent circuler divers métabolites. C’est par ces jonctions que les astrocytes évacuent vers les capillaires, le potassium extracellulaire excédentaire généré par une intense activité neuronale. A travers ce réseau d’actrocytes se propagerait par exemple, des vagues d’ions calcium dont l’effet régulateur pourrait se faire sentir dans un grand nombre de synapses en même temps. Les prolongements astrocytaires qui entourent les synapses pourraient ainsi exercer un contrôle plus global sur la concentration ionique et le volume aqueux dans les fentes synaptiques. Le réseau astrocytaire constituerait donc un système de transmission non-synaptique qui se superposerait au système neuronal pour jouer un rôle majeur de modulation des activités neuronales. A cet effet, et dans l’espoir d’éclairer les neurochirurgiens et les spécialistes qui s’intéressent aux transplantations et à une meilleure maîtrise du transport et fonctionnement de l’influx nerveux. Le présent travail apporte une approche entre le transport et les propriétés électroniques d’une jonction miniature, une ‘microjonction’, dont la nanotechnologie ne saurait se passer, l’usage de jonctions P-N, un semi-conducteur dopé P (ions positifs) et un dopé N (ions négatifs), est très utilisé pour tous les dispositifs de type diode car ne laissant passer le courant que dans un sens, ce genre de jonction fait aussi apparaître des propriétés optiques intéressantes.
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MENZIKOV, SERGEY A. "NEURONAL MULTIFUNCTIONAL ATPase". Biophysical Reviews and Letters 08, n.º 03n04 (diciembre de 2013): 213–27. http://dx.doi.org/10.1142/s1793048013300065.
Here, we review the properties of a suggested mechanism for a neural ATPase complex based on our recent experimental findings. The mechanism represents a multifunctional ATPase: an enzyme that is a chloride pump and a GABA receptor. This enables new views on the ways Cl - channel transports anions and its regulation by the intra- and extracellular ions and molecules (in particular by glucose, ATP, [Formula: see text]). The hydrolytic activity of this GABA A-coupled ATPase provides the [Formula: see text] transport process the energy and determines a certain direction of ions flux across neuronal membrane. This can help with the research regarding several diseases such as epilepsy. [Formula: see text]Special Issue Comment: This project is about a multifunctional ATPase complex. Experiments involving measuring & solving individual ATPases are related with the Special Issue about FRET experiments,1 about enzymes,2 and about treatments when solving single molecules.3,4 The model suggested here is simply tested with these experimental and mathematical methods.
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Kaye, D. M., S. D. Wiviott, L. Kobzik, R. A. Kelly y T. W. Smith. "S-nitrosothiols inhibit neuronal norepinephrine transport". American Journal of Physiology-Heart and Circulatory Physiology 272, n.º 2 (1 de febrero de 1997): H875—H883. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h875.
Although it has been recently shown that nitric oxide (NO) and its congeners (NO(x)), including nitrosothiols, may modify catecholamine turnover in the brain, it is not known whether NO(x) affect norepinephrine (NE) uptake by sympathetic neurons. The nitrosothiol NO donor S-nitroso-acetylpenicillamine (SNAP, 100 microM for 1 h) elicited a concentration-dependent reduction in desipramine-sensitive [3H]NE uptake into PC-12 cells (66 +/- 3%; P < 0.01) or cultured rat superior cervical ganglia (74 +/- 5%; P < 0.001), whereas desipramine-insensitive [3H]NE uptake was unaffected, indicating a selective effect on uptake-1-mediated transport. Short-term coculture of PC-12 cells with microvascular endothelial cells expressing the cytokine-inducible NO synthase (NOS2) also exhibited a reduction in [3H]NE uptake (33 +/- 3%, P < 0.001) that could be prevented by the addition of the NOS inhibitor N-monomethyl-L-arginine (L-NMMA, 1 mM). Endogenous production of NO(x) by nerve growth factor-pretreated PC-12 cells also exhibited an L-NMMA-inhibitable reduction in [3H]NE uptake. Whereas SNAP resulted in a 10-fold elevation of PC-12 guanosine 3',5'-cyclic monophosphate (cGMP) content (P < 0.01), its effect on [3H]NE uptake was not mimicked by exposure to 8-bromo-cGMP. However, the inhibitory effect of SNAP on uptake-1-mediated [3H]NE transport could be attenuated by 1 mM cysteine, a sulfhydryl compound that could act as a sink for NO(x)-mediated nitrosation reactions, although cysteine did not affect the increase in intracellular cGMP with SNAP. These data suggest that an endogenous NO(x) source(s) modifies the activity of the uptake-1 catecholamine transporter in postganglionic sympathetic neurons, which, as we demonstrate, express both NOS1 and NOS3 isoforms, possibly by S-nitrosothiol-mediated nitrosation of regulatory sites on the transporter.
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Perry, Rotem Ben-Tov y Mike Fainzilber. "Nuclear transport factors in neuronal function". Seminars in Cell & Developmental Biology 20, n.º 5 (julio de 2009): 600–606. http://dx.doi.org/10.1016/j.semcdb.2009.04.014.
Stiess, Michael y Frank Bradke. "Neuronal transport: myosins pull the ER". Nature Cell Biology 13, n.º 1 (12 de diciembre de 2010): 10–11. http://dx.doi.org/10.1038/ncb2147.
Staff, N. P., E. E. Benarroch y C. J. Klein. "Neuronal intracellular transport and neurodegenerative disease". Neurology 76, n.º 11 (14 de marzo de 2011): 1015–20. http://dx.doi.org/10.1212/wnl.0b013e31821103f7.
Brenner, S. R., N. P. Staff, E. E. Benarroch y C. J. Klein. "Neuronal intracellular transport and neurodegenerative disease". Neurology 77, n.º 21 (21 de noviembre de 2011): 1932. http://dx.doi.org/10.1212/wnl.0b013e318239bf96.
Bakshi, Rachit, Shuchi Mittal, Zhixiang Liao y Clemens R. Scherzer. "A Feed-Forward Circuit of EndogenousPGC-1αandEstrogen Related Receptor αRegulates the Neuronal Electron Transport Chain". Parkinson's Disease 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2405176.
Peroxisome proliferator-activated receptor γcoactivator 1α(PGC-1α) is a central regulator of cellular and mitochondrial metabolism. Cellular bioenergetics are critically important in “energy-guzzling” neurons, but the components and wiring of the transcriptional circuit through whichPGC-1αregulates the neuronal electron transport chain have not been established. This information may be vital for restoring neuronal bioenergetics gene expression that is compromised during incipient Parkinson’s neuropathology and in aging-dependent brain diseases. Here we delineate a neuronal transcriptional circuit controlled by endogenousPGC-1α. We show that a feed-forward circuit of endogenous neuronalPGC-1αand the orphan nuclear estrogen-related receptorα(ERRα) activates the nuclear-encoded mitochondrial electron transport chain.PGC-1αnot onlytrans-activated expression ofERRα, but also coactivatedERRαtarget genes in complexes I, II, IV, and V of the neuronal electron transport chain via association with evolutionary conservedERRαpromoter binding motifs. Chemical activation of this transcriptional program induced transcription of the neuronal electron transport chain. These data highlight a neuronal transcriptional circuit regulated byPGC-1αthat can be therapeutically targeted for Parkinson’s and other neurodegenerative diseases.
MacAskill, A. F. N. "Control of neuronal mitochondrial transport". Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19495/.
Synapses consume large amounts of energy, and energy supply to synaptic sites is critical for their proper function. Most energy in the brain is supplied by mitochondria, organelles efficient at utilising oxygen and substrates such as glucose and pyruvate to produce cellular energy in the form of ATP. Due to the large size of many neurons - which precludes the rapid diffusion of ATP from one side of the cell to the other - mitochondria must be positioned close to activated synaptic sites. There must therefore be transport pathways that allow mitochondria to move throughout the cell. As patterns of neuronal activity are constantly changing, these transport pathways must also be able to be controlled on rapid timescales. The molecular mechanisms that underlie the movement of mitochondria have remained elusive. In this study, a mechanism for coupling mitochondria to the microtubule based transport pathway was characterised. Miro1, a mitochondrial membrane protein, was shown to link mitochondria to kinesin motor proteins in a complex with the adaptor protein Trak2. Varying the levels of Miro1 in neurons altered the ability of mitochondria to move throughout the cell. To provide energy to activated synapses, there must be signals that can control mitochondrial movement. This study describes two mechanisms that allow this control. First, GTP dependent recruitment of the adaptor protein Trak2 is shown to control the number of mitochondria transported into neuronal processes. Second, calcium entry through NMDA receptors upon synaptic activation causes a localised stopping of mitochondria around the active sites. This is shown to be caused by calcium inhibiting the Miro1:kinesin interaction and results in recruitment of mitochondria to activated synapses. This study provides a mechanism where local energy demand can be spatially linked to energy production, by controlling mitochondrial transport through the mitochondrial membrane protein Miro1.
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Mahato, Deependra. "Mutation of Polaris, an Intraflagellar Transport Protein, Shortens Neuronal Cilia". Thesis, University of North Texas, 2005. https://digital.library.unt.edu/ark:/67531/metadc4856/.
Primary cilia are non-motile organelles having 9+0 microtubules that project from the basal body of the cell. While the main purpose of motile cilia in mammalian cells is to move fluid or mucus over the cell surface, the purpose of primary cilia has remained elusive for the most part. Primary cilia are shortened in the kidney tubules of Tg737orpk mice, which have polycystic kidney disease due to ciliary defects. The product of the Tg737 gene is polaris, which is directly involved in a microtubule-dependent transport process called intraflagellar transport (IFT). In order to determine the importance of polaris in the development of neuronal cilia, cilium length and numerical density of cilia were quantitatively assessed in six different brain regions on postnatal days 14 and 31 in Tg737orpk mutant and wildtype mice. Our results indicate that the polaris mutation leads to shortening of cilia as well as decreased percentage of ciliated neurons in all brain regions that were quantitatively assessed. Maintainance of cilia was especially affected in the ventromedial nucleus of the hypothalamus. Furthermore, the polaris mutation curtailed cilium length more severely on postnatal day 31 than postnatal day 14. These data suggests that even after ciliogenesis, intraflagellar transport is necessary in order to maintain neuronal cilia. Regional heterogeneity in the effect of this gene mutation on neuronal cilia suggests that the functions of some brain regions might be more compromised than others.
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Chen, Liang. "Single molecule and single particle studies of neuronal axonal transport /". May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Johnson, Christopher M. "Investigating the Slow Axonal Transport of Neurofilaments: A Precursor for Optimal Neuronal Signaling". Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1452018547.
Cette these constituee de deux parties aborde l'efficacite du parallelisme suivant deux approches complementaires. Dans la premiere partie l'architecture neuronale est consideree comme une architecture massivement parallele sans contrainte de communication et deux methodes fondees sur le calcul neuronal appliquees a l'optimisation combinatoire sont etudiees. La methodologie de l'optimisation par les reseaux de neurones aleatoires est developpee et une methode deterministe utilisant des reseaux dynamiques est proposee pour le probleme du stable maximum. Dans le second travail l'approche de la machine de boltzmann est utilisee pour resoudre les problemes de partitionnement et de couverture. Dans la seconde partie l'efficacite du parallelisme est etudiee relativement au cout de la communication. Pour les applications executees dans les reseaux de stations de travail le niveau optimal du parallelisme est calcule en fonction des parametres du systeme et des besoins de communication des taches constituant l'application. Dans le dernier travail les probabilites de perte des paquets dans les reseaux atm sont calculees par l'approximation de diffusion stationnaire et transitoire sous la condition de charge hautement variable.
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Coats, Charles Jason. "Development of primary neuronal culture of embryonic rabbit dorsal root ganglia for microfluidic chamber analysis of axon mediated neuronal spread of Bovine Herpesvirus type 1". Thesis, Manhattan, Kan. : Kansas State University, 2010. http://hdl.handle.net/2097/4115.
Li, Yunyun [Verfasser] y Peter [Akademischer Betreuer] Hänggi. "Noise assisted transport in artificial channels and neuronal membranes / Yunyun Li. Betreuer: Peter Hänggi". Augsburg : Universität Augsburg, 2011. http://d-nb.info/1077700296/34.
Doctor of Philosophy Department of Anatomy and Physiology Timothy I. Musch Nitric oxide (NO) is synthesized via distinct NO synthase (NOS) enzymes and constitutes an essential cardiovascular signaling molecule. Whereas important vasomotor contributions of endothelial NOS (eNOS) have been well-described, the specific vasomotor contributions of nNOS-derived NO in healthy subjects during exercise are unknown. The purpose of this dissertation is to test the global hypothesis that nNOS-derived NO is a critical regulator of exercising skeletal muscle vascular control. Specifically, we utilized the selective nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) to investigate the effects of nNOS-derived NO on skeletal muscle vascular function within established rodent models of exercise performance. The first investigation (Chapter 2) identifies that nNOS inhibition with SMTC increases mean arterial pressure (MAP) and reduces rat hindlimb skeletal muscle blood flow at rest whereas there are no effects during low-speed (20 m/min) treadmill running. In Chapter 3 it is reported that nNOS inhibition with SMTC reduces blood flow during high-speed treadmill running (>50 m/min) with the greatest relative effects found in highly glycolytic fast-twitch muscles and muscle parts. Chapter 4 demonstrates that nNOS-derived NO modulates contracting skeletal muscle blood flow (increases), O2 consumption (VO2, increases), and force production (decreases) in the rat spinotrapezius muscle and thus impacts the microvascular O2 delivery-VO2 ratio (which sets the microvascular partial pressure of O2, PO2mv, and represents the pressure head that drives capillary-myocyte O2 diffusion). In Chapter 5 we report that systemic administration of the selective nNOS inhibitor SMTC does not impact lumbar sympathetic nerve discharge. This reveals that the SMTC-induced peripheral vascular effects described herein reflect peripheral nNOS-derived NO signaling as opposed to centrally-derived regulation. In conclusion, nNOS-derived NO exerts exercise-intensity and muscle fiber-type selective peripheral vascular effects during whole-body locomotor exercise. In addition, nNOS-derived NO modulates skeletal muscle contractile and metabolic function and, therefore, impacts the skeletal muscle PO2mv. These data identify novel integrated roles for nNOS-derived NO within healthy skeletal muscle and have important implications for populations associated with reduced NO bioavailability and/or impaired nNOS structure and/or function specifically (e.g., muscular dystrophy, chronic heart failure, advanced age, etc.).
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Naudon, Laurent. "Recherche d'une participation du transporteur neuronal de la dopamine et du transporteur vésiculaire à l'adaptation neuronale". Rouen, 1994. http://www.theses.fr/1994ROUES066.
L'ensemble des résultats que nous avons obtenus semblent indiquer que le transporteur neuronal de la dopamine et le transporteur vésiculaire des monoamines, malgré leurs rôles essentiels dans la transmission synaptique, ne participent que faiblement à l'adaptation des neurones dopaminergiques
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Daoust, Alexia. "IRM du manganèse (MEMRI) : couplage à l'imagerie chimique par microsonde synchrotron pour optimiser l'imagerie fonctionnelle du transport neuronal". Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00770158.
Résumé Le manganèse (Mn2+) est un élément essentiel du corps humain. Ses propriétés paramagnétiques permettent son utilisation comme agent de contraste pour l'IRM (Mn-MRI ou MEMRI). Analogue du calcium (Ca2+), il pénètre les neurones essentiellement par les canaux calciques. Il est ensuite transporté le long des microtubules jusqu'aux synapses où il est libéré, puis capturé par les autres neurones. Ainsi, il peut rendre compte du transport axonal antérograde et rétrograde. L'approche MEMRI peut ainsi apporter des informations uniques sur la connectivité fonctionnelle cérébrale. Toutefois, deux problèmes limitent l'emploi de ce puissant outil d'imagerie in vivo : (i) A doses élevées, le Mn2+ est toxique pour l'organisme et peut provoquer une atteinte grave du système nerveux central, appelé manganisme. Les niveaux et les mécanismes de toxicité sont mal connus. (ii) Le mode de transport du manganèse dans l'approche MEMRI est mal connu. Afin d'apporter des éléments de réponse à ces deux problèmes, nous avons entrepris une étude couplant IRM et microscopie synchrotron pour mieux comprendre le comportement du Mn2+ in vivo. Nous avons précisé les distributions cellulaire et sub-cellulaire du Mn et d'autres métaux pour un modèle de cellules de type neuronal (lignée de neuroblastome N2A), pour des cultures primaires de neurones hippocampiques, mais aussi au niveau de coupes d'hippocampe de rats. En parallèle, nous avons étudié les effets du Mn sur le métabolisme cérébral par une technique de RMN-HRMAS du proton. Pour compléter ce travail, nous avons mis en œuvre l'imagerie MEMRI chez les souris KO MAP6 présentant un déficit d'une protéine stabilisatrice des microtubules pour évaluer la connectivité fonctionnelle du tract thalamo-cortical. Mots clés Hippocampe, MAP6, manganèse, métabolisme, métal, neurone, MRI, rongeurs, synchrotron.
International Conference on Biological Membranes (11th 1985 Crans, Switzerland). Ion channels in neural membranes: Proceedings of the 11th International Conference on Biological Membranes held at Crans-sur-Sierre, Switzerland, June 10-14, 1985. Editado por Ritchie J. Murdoch, Keynes R. D y Bolis Liana. New York: A.R. Liss, 1986.
J, Alvarez-Leefmans F., Russell John M. 1942- y International Brain Research Organization. Congress, eds. Chloride channels and carriers in nerve, muscle, and glial cells. New York: Plenum Press, 1990.
Capítulos de libros sobre el tema "Transport neuronal":
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Knight, Adam L., Yanmin Chen, Tao Sun y Zu-Hang Sheng. "Neuronal Mitochondrial Transport". En The Functions, Disease-Related Dysfunctions, and Therapeutic Targeting of Neuronal Mitochondria, 166–85. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781119017127.ch7.
Voelzmann, André y Natalia Sanchez-Soriano. "Drosophila Primary Neuronal Cultures as a Useful Cellular Model to Study and Image Axonal Transport". En Methods in Molecular Biology, 429–49. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_23.
AbstractThe use of primary neuronal cultures generated from Drosophila tissue provides a powerful model for studies of transport mechanisms. Cultured fly neurons provide similarly detailed subcellular resolution and applicability of pharmacology or fluorescent dyes as mammalian primary neurons. As an experimental advantage for the mechanistic dissection of transport, fly primary neurons can be combined with the fast and highly efficient combinatorial genetics of Drosophila, and genetic tools for the manipulation of virtually every fly gene are readily available. This strategy can be performed in parallel to in vivo transport studies to address relevance of any findings. Here we will describe the generation of primary neuronal cultures from Drosophila embryos and larvae, the use of external fluorescent dyes and genetic tools to label cargo, and the key strategies for live imaging and subsequent analysis.
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Atkin, Talia A., Andrew F. MacAskill y Josef T. Kittler. "Neuronal Mitochondrial Transport and Dysfunction". En Mitochondrial Dysfunction in Neurodegenerative Disorders, 157–73. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-701-3_10.
Stephenson, F. Anne y Kieran Brickley. "Mechanisms of Neuronal Mitochondrial Transport". En Folding for the Synapse, 105–19. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7061-9_6.
Deitmer, Joachim W. "pH regulation and acid/base-mediated transport in glial cells". En Glial ⇔ Neuronal Signaling, 263–77. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_10.
Ledeen, R. W., D. A. Aquino, M. Sbaschnig-Agler, C. M. Gammon y K. K. Vaswani. "Fundamentals of Neuronal Transport of Gangliosides. Functional Implications". En Gangliosides and Modulation of Neuronal Functions, 259–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71932-5_21.
Caputto, R., B. L. Caputto, M. S. Domowicz y S. C. Kivatinitz. "Gangliosides: Biosynthesis, Transport and Location in the Plasma Membrane". En Gangliosides and Modulation of Neuronal Functions, 251–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71932-5_20.
Pichiule, P., J. C. Chavez, R. J. Przybylski y J. C. LaManna. "Increase of Neuronal Nitric Oxide Synthase during Chronic Hypoxia". En Oxygen Transport to Tissue XX, 319–23. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4863-8_37.
Miller, Richard J. "Modulation and Functions of Neuronal Ca2+ Permeable Channels". En Calcium Transport and Intracellular Calcium Homeostasis, 3–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_1.
Aquino, D. A., M. A. Bisby y R. W. Ledeen. "Axonal Transport of Gangliosides and Neutral Glycolipids in the Peripheral Nervous System. Identification of Ganglioside Types in Motoneurons of the PNS". En Gangliosides and Neuronal Plasticity, 161–69. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_14.
Actas de conferencias sobre el tema "Transport neuronal":
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Zhu, Liang y Robert Flower. "Role of Vasomotion in Control of Retina Edema in Diabetic Retinopathy: Quantification of Fluid Transport Through Retinal Capillaries". En ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-189507.
Diabetic retinopathy refers to diabetes-related complications in the retina, It is a progressive disease and its symptoms in the eyes can vary from non-vision threatening to vision loss, and it can lead to permanent damage to the neuronal retinal tissue. The irreversible nature of the damage suggests that prevention of diabetes by eliminating risk factors and early screening are the cornerstone of relevant treatment to stop or limit visual damage in those patients.
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Smith, Jennifer A., Gregoriy Smiyun, Leslie Wilson, Stuart Feinstein y Mary Ann Jordan. "Abstract 5294: Inhibition of mitochondrial transport in neuronal cells by microtubule-targeting drugs eribulin, ixabepilone, paclitaxel, and vincristine". En Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5294.
Lee, Sung Jin, Jingjing Sun, Michael King, Huikai Xie y Malisa Sarntinoranont. "Viscoelastic Property Changes of Acute Rat Brain Tissue Slices as a Function of Cell Viability". En ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53909.
Changes in mechanical properties within brain tissues after losses in cell viability have not been well investigated. Lack of oxygen and nutrient transport can induce hypoxic neuronal injury and increase cell membrane permeability, and cell membranes and matrix components can lose their structural and mechanical integrity. These physical changes may have an effect on mechanical properties of brain tissue [1]. In this study, the viscoelastic behavior of two anatomical regions (cerebral cortex and hippocampus) in acute rat brain tissue slices were measured as a function of cell viability using indentation combined with optical coherence tomography (OCT). Neuronal viability in brain tissue slices was determined by measuring Fluoro-Jade C (FJC) staining to assay neuronal death or degeneration as a function of incubation time. OCT-measured deformation depths were compared with finite element (FE) simulations to estimate the relaxation of shear modulus. Measured equilibrium shear modulus (μ∞) after 8 hrs incubation was lower than μ∞ measured after 2 hrs incubation in the cerebral cortex (μ∞, 2hrs = 225 Pa, μ∞, 8hrs = 62 Pa) and hippocampus regions (μ∞, 2hrs = 170 Pa, μ∞, 8hrs = 33 Pa). Instantaneous shear modulus (μ0) after 8 hrs incubation was also an order of magnitude lower than μ0 after 2 hrs incubation in cortex (μ0, 2hrs = 1600 Pa, μ0, 8hrs = 100 Pa) and hippocampus regions (μ0, 2hrs = 370 Pa, μ0, 8hrs = 70 Pa). The results of this study provide a timeline for measuring mechanical properties of brain tissues ex vivo and provide better understanding of changes in brain modulus after injury or cell death.
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Stork, Larissa Rosa, Lucca Stephani Ribeiro, Izabella Savergnini Deprá, Luísa D’Ávila Camargo y Maria Angélica Santos Novaes. "Tau protein and its role in Alzheimer’s disease physiopathology: a literature review". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.132.
Background: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a double proteinopathy: deposition of amyloid-β into plaques and hyperphosphorylation of Tau protein. Objectives: To understand the genetic and molecular aspects of Tau protein and its relationship with Alzheimer’s disease. Methods: We conducted a systematic literature search using Pubmed/ MEDLINE and ClinicalKey databases, applying the descriptors: “Alzheimer Disease” AND “Tau proteins’’ AND Tauopathies, during July and August of 2020. The inclusion criteria were English and Portuguese articles published between 2015 and 2020, with human limited study and free full text, excluding images, books, clinical tests, and narrative reviews. After analyzing titles and abstracts, we selected 12 articles and included 7 additional studies. Results: Mapt, the encoder gene of Tau, is located in the 17q21.3 locus and presents 16 exons that, when transcripted, originates 12 copies of mRNA by alternative splicing and 6 Tau’s isoforms. Tau is a microtubule-associated protein (MAP) responsible for cellular cytoskeleton stabilization and maintenance, promoting neuronal axonal transport. A kinase-phosphatase imbalance turns Tau hyperphosphorylated, disassociating it from tubulin and grouping it into insoluble paired helical filaments, which originates neurofibrillary tangles. The tauopathy’s progress causes neurotransmitter destabilization and neuronal death, inducing AD symptomatic manifestations. Conclusions: Due to the gradual worsening of the disease to more debilitating stages, studies focused on deepening the knowledge of genetic and molecular aspects of Tau protein are viable and promising alternatives to improve the quality of patient’s lives.
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Brooks, Joseph Bruno Bidin. "De novo variant in the MAPK8IP3 gene in the differential diagnosis of global development delay. Case report." En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.181.
Context: The global development delay has a high prevalence and heterogeneity in the world population. With the advancement of technology and detection of pathogenic variants detected by sequencing the exome, genes related to global developmental delay could be identified and collaborate for further clinical clarification. Among the studied genes, the MAPK8IP3 gene, became an attractive candidate due to its performance in neuronal axonal transport in vertebrates and invertebrates. This case report was approved by the Ethics Committee of Universidade Metropolitana de Santos. Case Report: The present case refers to a 6-year-old male patient presenting with a clinical picture of global developmental delay without bodily dysmorphia. Cerebellar ataxia, muscle hypotonia and intellectual impairment are important clinical impairments. Skull MRI and complementary exams were normal. The genetic study showed a new and heterozygous pathogenic variant in the MAPK8IP3 gene. Conclusions: Symptomatic treatment with multiprofessional rehabilitation was instituted with partial improvement of symptoms.
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Garrido Rodriguez, Maria Concepcion. "Análisis de la calidad del servicio en el transporte público mediante redes neuronales artificiales". En CIT2016. Congreso de Ingeniería del Transporte. Valencia: Universitat Politècnica València, 2016. http://dx.doi.org/10.4995/cit2016.2016.4120.
El éxito de un servicio de transporte público reside en su capacidad para captar nuevos pasajeros y de fidelizar el uso de los actuales. De ahí que las administraciones y los gestores de transporte se preocupen cada vez más por conocer cuál es la calidad percibida por los usuarios. Aunque existen numerosos métodos matemáticos que ya han sido utilizados para analizar la calidad del servicio en el transporte público, es necesario seguir avanzando en el estudio de nuevas técnicas que sean válidas para su estudio. En esta ponencia se aplica la técnica de las redes neuronales artificiales al estudio de la calidad del servicio en el transporte público. La metodología novedosa desarrollada al aplicar las redes neuronales artificiales mitiga considerablemente las principales limitaciones que éstas presentan, por lo que además de aportar una nueva herramienta para análisis de la calidad del servicio en el transporte público, pone a disposición de los especialistas en esta técnica un nuevo procedimiento de aplicación de las redes neuronales artificiales aplicable a cualquier campo de estudio en el que esta técnica sea aplicada.DOI: http://dx.doi.org/10.4995/CIT2016.2016.4120
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Mudrakola, Harsha V., Chengbiao Wu, Kai Zhang y Bianxiao Cui. "Single Molecule Imaging of Axonal Transport in Live Neurons". En Laser Science. Washington, D.C.: OSA, 2009. http://dx.doi.org/10.1364/ls.2009.lsthb3.
Yang, Chun-Lin, Nandan Shettigar y C. Steve Suh. "A Proposition for Describing Real-World Network Dynamics". En ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-73360.
Abstract This study presents a proposition for describing the dynamics of real-world networks under the general framework of complex networks. Outward behaviors of complex networks are the manifestation of the coupled dynamics at the macroscopic level and the individual dynamics at the microscopic level. At the macroscopic level a law of coupling governs the interactions of network constituents. At the microscopic level, the dynamics of individual constituent is defined by energy that follows normal distribution. Constituent dynamics are bounded by physical constraints. Consequently, network dynamics can be quantified using information entropy which is a function of constituent energy. In real-world networks, differences between individual constituents exist due to differing mechanical properties and dynamics. Consequently, network dynamics are of different layers and hierarchies. Construct of network governing equations formulated under the general framework of complex networks are demonstrated using two real-world networks — a brain network and a lymph node network. Brain network is constructed by the neurons that each connected by the synapse. Brain network dynamics is composed by the law of coupling defined by the synaptic dynamics through the transmitting of neurotransmitters that couples the individual neuron dynamics. Since different classifications exist among neurotransmitters and neurons, the post synaptic neuron can present either inhibitory or excitatory action. The inhibitory and excitatory behavior of the neurons changes the mechanical properties of each neuron and further alters the brain network dynamics. Consequently, the brain network emerges dynamics with different layers. Lymph node network drains fluid from blood vessels, filter the lymph (the interstitial fluid lymphatic system collects from the blood circulation) through lymph nodes, and transport the lymph back to the blood circulation. Lymph node dynamics is composed by the dynamics of lymph transportation along the lymph node network and the individual lymph node dynamics that involves lymphocytes-pathogens interactions (adaptive immune response). In each lymph node, lymphocytes fight off the pathogens which also emerges a network dynamics such as the interaction between T cells and HIV viruses. Finally, the lymph is collected from each lymph nodes and drained back to the blood circulation. As a result, the lymph node network has the dynamics of different hierarchies where the lymphocytes-pathogens dynamics exists within each lymph node at the lower hierarchy is further under the influence of the lymph transportation dynamics among the whole lymph node network on the higher hierarchy. Since the constituent dynamics of the brain network and lymph node network can be defined by energy that follows normal distribution and both are bounded by physical constraints, the network dynamics of both cases can be quantified through information entropy. Features pertaining to the global as well as individual constituent dynamics of the networks are identified that are insightful to the control of such complex networks.
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Schmitt-Böhrer, A., JF Kolter, A. Kreis, C. Hamann, C. Bodden, N. Sachser, E. Asa y K.-P. Lesch. "Impact of different life histories on neuronal morphology in serotonin transporter deficient mice". En Abstracts of the 2nd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402985.
Becker, Nicole Bernd, Allan Marinho Alcará, Isadora Ghilardi, Vitoria Pimentel, Giulia Pinzetta, Laura Provenz, Gabriel Leal et al. "Mesenchymal stem cells modulate the gene expression of cationchloride co-transporter KCC2 in epileptogenesis". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.693.
Background: Temporal Lobe Epilepsy (TLE), by firing of neuronal populations, leads to spontaneous and recurrent seizures1 . As 30% of TLE patients do not respond to pharmacotherapy2,3, it is necessary to search for alternatives. Mesenchymal stem cells (MSCs) are an attractive approach in this context, due to their less invasive character and its ability to modulate diseased niches. Objective: Analyze the gene expression related to the cation-chloride cotransporter KCC2 in TLE induced by pilocarpine model in rats. Design and Setting: Experimental study, Brain Institute of Rio Grande do Sul. Methods: MSCs were extracted from the bone marrow of Wistar rats, cultured and transplanted intravenously and intranasally into healthy and epileptic Wistar rats. Results: It was observed a decrease in the expression of KCC2 in the brain of the animals at 1-day post-transplant, which refers to a down-regulation, and an increase at 7 days post-transplant, representing an up-regulation. The loss of function of KCC2 decreases the release of chloride with difficulty in inhibiting GABAergic inhibition, resulting in hyperexcitability of neuronal circuits. In this case, MSCs can promote rearrangement in gamma-aminobutyric acid-mediated inhibition, reducing hyperexcitability and hypersynchronicity. Hence, KCC2 down-regulation is associated with epileptiform activity, while up-regulation can be related to the MSCs effects. Also, KCC2 expression showed a kind of pattern at 1-day post- transplant in both routes of administration, providing the possibility that KCC2 can be explored as a biomarker for epilepsy. Conclusion: KCC2 is an important target for epilepsy, as well MSCs have a modulatory function on the levels of the expression of this gene in animals induced to status epilepticus by pilocarpine.
