Academic literature on the topic 'Neuronal NOS'
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Journal articles on the topic "Neuronal NOS"
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Lapointe, Jérome, Monica Roy, Isabelle St-Pierre, Sarah Kimmins, Danny Gauvreau, Leslie A. MacLaren, and Jean-François Bilodeau. "Hormonal and Spatial Regulation of Nitric Oxide Synthases (NOS) (Neuronal NOS, Inducible NOS, and Endothelial NOS) in the Oviducts." Endocrinology 147, no. 12 (December 1, 2006): 5600–5610. http://dx.doi.org/10.1210/en.2005-1548.
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Nitric oxide (NO) is a free radical produced by the action of NO synthases (NOS) and is known to be involved in the regulation of many reproductive events that occur in the oviducts. The oviducts are highly specialized organs that play crucial roles in reproduction by providing an optimal environment for the final maturation of gametes, fertilization, and early embryo development. In this study, we analyzed the expression, hormonal regulation, and cellular distribution of neuronal, inducible, and endothelial NOS in different bovine oviduct segments to better understand the roles played by these enzymes in oviductal functions in vivo. Quantitative RT-PCR analysis revealed that NOS isoforms are hormonally regulated and differentially expressed along the oviduct throughout the estrous cycle. All NOS were highly expressed around the time of estrus, and immunohistochemistry studies determined that neuronal NOS, inducible NOS (iNOS), and endothelial NOS are differentially distributed in cells along the oviduct. Interestingly, our results showed that estradiol selectively up-regulates iNOS expression in the oviduct during the periovulatory period corresponding to the window of ovulation, oocyte transport, and fertilization. The resulting NO production by this high-output NOS may be of crucial importance for reproductive events that occur in the oviduct. This study provided the first demonstration that NO production is hormonally regulated in the mammalian oviducts in vivo. Our results suggest that neuronal NOS, iNOS, and endothelial NOS contribute to oviductal functions in a timely and site-specific manner.
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KOHN, A. B., L. L. MOROZ, J. M. LEA, and R. M. GREENBERG. "Distribution of nitric oxide synthase immunoreactivity in the nervous system and peripheral tissues of Schistosoma mansoni." Parasitology 122, no. 1 (January 2001): 87–92. http://dx.doi.org/10.1017/s0031182000007022.
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The distribution of nitric oxide synthase (NOS) immunoreactivity and putative NOS activity in adult Schistosoma mansoni was analysed using 3 different types of NOS antibodies and NADPH-diaphorase histochemistry. Although potential involvement of the gaseous radical nitric oxide (NO) in host response to infection by schistosomes has been suggested, there is little or no information available regarding the role, or even the presence, of the NO pathway in schistosomes themselves. Here, we demonstrate that antibodies against neuronal NOS (nNOS) and inducible NOS (iNOS) isoforms stain adult worms with distinctive patterns; anti-endothelial NOS (eNOS) shows no selective labelling. nNOS-like immunoreactivity is found in the main nerve cords and the peripheral nervous system. Putative sensory neurons with apical neuronal processes leading to the tegument of male worms are also immunoreactive for nNOS. Anti-iNOS labels a variety of predominantly non-neuronal tissues, showing intense labelling at or near the surface of the worm and in components of the gastrointestinal tract. The distribution of NADPH-diaphorase reactivity (a histochemical marker of NOS), is generally similar to the pattern of NOS immunoreactivity, including labelling of neuronal-like cells as well as developing eggs. These results suggest that an NOS-like enzyme is present in S. mansoni, and indicate potential roles for the different NOS isoforms in neuronal signalling, reproduction and development.
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Premaratne, Shyamal, Chun Xue, John M. McCarty, Muhammad Zaki, Robert W. McCuen, Roger A. Johns, Wolfgang Schepp, et al. "Neuronal nitric oxide synthase: expression in rat parietal cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 2 (February 1, 2001): G308—G313. http://dx.doi.org/10.1152/ajpgi.2001.280.2.g308.
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Nitric oxide synthases (NOS) are enzymes that catalyze the generation of nitric oxide (NO) from l-arginine and require nicotinamide adenine dinucleotide phosphate (NADPH) as a cofactor. At least three isoforms of NOS have been identified: neuronal NOS (nNOS or NOS I), inducible NOS (iNOS or NOS II), and endothelial NOS (eNOS or NOS II). Recent studies implicate NO in the regulation of gastric acid secretion. The aim of the present study was to localize the cellular distribution and characterize the isoform of NOS present in oxyntic mucosa. Oxyntic mucosal segments from rat stomach were stained by the NADPH-diaphorase reaction and with isoform-specific NOS antibodies. The expression of NOS in isolated, highly enriched (>98%) rat parietal cells was examined by immunohistochemistry, Western blot analysis, and RT-PCR. In oxyntic mucosa, histochemical staining revealed NADPH-diaphorase and nNOS immunoreactivity in cells in the midportion of the glands, which were identified as parietal cells in hematoxylin and eosin-stained step sections. In isolated parietal cells, decisive evidence for nNOS expression was obtained by specific immunohistochemistry, Western blotting, and RT-PCR. Cloning and sequence analysis of the PCR product confirmed it to be nNOS (100% identity). Expression of nNOS in parietal cells suggests that endogenous NO, acting as an intracellular signaling molecule, may participate in the regulation of gastric acid secretion.
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Pigott, B., K. Bartus, and J. Garthwaite. "On the selectivity of neuronal NOS inhibitors." British Journal of Pharmacology 168, no. 5 (February 20, 2013): 1255–65. http://dx.doi.org/10.1111/bph.12016.
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Jackson, Claire L., Jane S. Lucas, Woolf T. Walker, Holly Owen, Irnthu Premadeva, and Peter M. Lackie. "Neuronal NOS localises to human airway cilia." Nitric Oxide 44 (January 2015): 3–7. http://dx.doi.org/10.1016/j.niox.2014.11.003.
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O'Dell, T., P. Huang, T. Dawson, J. Dinerman, S. Snyder, E. Kandel, and M. Fishman. "Endothelial NOS and the blockade of LTP by NOS inhibitors in mice lacking neuronal NOS." Science 265, no. 5171 (July 22, 1994): 542–46. http://dx.doi.org/10.1126/science.7518615.
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Idigo, Winifred O., Svetlana Reilly, Mei Hua Zhang, Yin Hua Zhang, Raja Jayaram, Ricardo Carnicer, Mark J. Crabtree, Jean-Luc Balligand, and Barbara Casadei. "Regulation of Endothelial Nitric-oxide Synthase (NOS)S-Glutathionylation by Neuronal NOS." Journal of Biological Chemistry 287, no. 52 (October 22, 2012): 43665–73. http://dx.doi.org/10.1074/jbc.m112.412031.
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Kourosh-Arami, Masoumeh, Nasrin Hosseini, Monireh Mohsenzadegan, Alireza Komaki, and Mohammad Taghi Joghataei. "Neurophysiologic implications of neuronal nitric oxide synthase." Reviews in the Neurosciences 31, no. 6 (August 27, 2020): 617–36. http://dx.doi.org/10.1515/revneuro-2019-0111.
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AbstractThe molecular and chemical properties of neuronal nitric oxide synthase (nNOS) have made it a key mediator in many physiological functions and signaling transduction. The NOS monomer is inactive, but the dimer form is active. There are three forms of NOS, which are neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) nitric oxide synthase. nNOS regulates nitric oxide (NO) synthesis which is the mechanism used mostly by neurons to produce NO. nNOS expression and activation is regulated by some important signaling proteins, such as cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB), calmodulin (CaM), heat shock protein 90 (HSP90)/HSP70. nNOS-derived NO has been implicated in modulating many physiological functions, such as synaptic plasticity, learning, memory, neurogenesis, etc. In this review, we have summarized recent studies that have characterized structural features, subcellular localization, and factors that regulate nNOS function. Finally, we have discussed the role of nNOS in the developing brain under a wide range of physiological conditions, especially long-term potentiation and depression.
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Fabricius, M., I. Rubin, M. Bundgaard, and M. Lauritzen. "NOS activity in brain and endothelium: relation to hypercapnic rise of cerebral blood flow in rats." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (November 1, 1996): H2035—H2044. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h2035.
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We examined whether attenuation of the hypercapnic increase of cerebral blood flow (CBF) associated with nitric oxide synthase (NOS) inhibition is related to local neuronal or aortic endothelial NOS activity or local endothelial/neuronal NOS-dependent vasodilation. Halothane-anesthetized rats were ventilated, and CBF was measured by laser-Doppler flowmetry over the parietal and cerebellar cortex. Intravenous N omega-nitro-L-arginine (L-NNA; 30 mg/kg) inhibited brain and aortic NOS activity by 67-70%. Topical L-NNA (1 mM) inhibited brain NOS activity by 91-94%, whereas aortic NOS activity remained constant. In contrast, intravenous L-NNA attenuated the hypercapnic CBF rise much more efficiently than topical L-NNA. 7-Nitroindazole, another NOS inhibitor, attenuated endothelial and neuronal NOS activity equally well and inhibited the hypercapnic CBF increase as effectively as L-NNA. Topical L-NNA and 7-nitroindazole abolished local endothelial NOS-dependent vasodilation after 15 min, whereas hypercapnic CBF was only slightly reduced. L-NNA injected into the tissue abolished neuronal NOS-dependent vasodilation, whereas hypercapnic CBF was unchanged. The findings suggest that local NOS activity, whether neuronal or endothelial, is unimportant for the hypercapnic rise of CBF.
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Li, Huiying, Joumana Jamal, Carla Plaza, Stephanie Hai Pineda, Georges Chreifi, Qing Jing, Maris A. Cinelli, Richard B. Silverman, and Thomas L. Poulos. "Structures of human constitutive nitric oxide synthases." Acta Crystallographica Section D Biological Crystallography 70, no. 10 (September 27, 2014): 2667–74. http://dx.doi.org/10.1107/s1399004714017064.
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Mammals produce three isoforms of nitric oxide synthase (NOS): neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). The overproduction of NO by nNOS is associated with a number of neurodegenerative disorders; therefore, a desirable therapeutic goal is the design of drugs that target nNOS but not the other isoforms. Crystallography, coupled with computational approaches and medicinal chemistry, has played a critical role in developing highly selective nNOS inhibitors that exhibit exceptional neuroprotective properties. For historic reasons, crystallography has focused on rat nNOS and bovine eNOS because these were available in high quality; thus, their structures have been used in structure–activity–relationship studies. Although these constitutive NOSs share more than 90% sequence identity across mammalian species for each NOS isoform, inhibitor-binding studies revealed that subtle differences near the heme active site in the same NOS isoform across species still impact enzyme–inhibitor interactions. Therefore, structures of the human constitutive NOSs are indispensible. Here, the first structure of human neuronal NOS at 2.03 Å resolution is reported and a different crystal form of human endothelial NOS is reported at 1.73 Å resolution.
Dissertations / Theses on the topic "Neuronal NOS"
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Papale, Davide. "Oxygen activation during neuronal NOS reaction." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/12755.
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Nitric oxide synthase (NOS) catalyzes nitric oxide (NO) production in a two step reaction. The first step involves L-arginine being oxidised to NG-hydroxy-L-arginine (NOHA) that remains bound to the enzyme before it is oxidised to NO and L-citrulline in the second step. The three mammalian isozymes are homodimeric enzymes and each subunit is composed of a reductase and an oxygenase domain. The oxygenase domain contains the arginine binding site, one cysteine ligated heme thiolate, and one H4B molecule ((6R)-5,6,7,8-Tetrahydrobiopterin). The enzyme’s substrates are O2, L-arginine (or NOHA) and NADPH. H4B is an essential cofactor for NO production by NOS and its roles are in dimerization and as redox cofactor. The mechanism of the reaction between L-arg and oxygen in the active site is currently uncertain. Therefore in order to alter the course of the reaction site-directed mutagenesis was conducted: Glycine 586 of nNOS was replaced by a serine residue (G586S nNOSoxy) and expressed and purified from E.coli. Stopped flow kinetic experiments showed the formation of a novel reaction intermediate during G586S nNOSoxy catalysis in the presence of H4B and substrate, subsequent to the formation of the oxy-ferrous compound. It is suggested that the new intermediate is formed as a transient along the path of the NO production reaction and has spectroscopic resemblance to the putative P450 active species, the oxy-ferryl compound. Crystals of the G586S mutant have been obtained and the solved x-ray structure shows the newly introduced serine residue pointing toward the guanidinium group of L-arg, reinforcing its involvement in the stabilization of a reaction intermediate.
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Sobolewska-Stawiarz, Anna. "Probing the dynamics and conformational landscape of neuronal nitric oxide synthase." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/probing-the-dynamics-and-conformational-landscape-of-neuronal-nitric-oxide-synthase(82903814-5474-42e3-9339-d9a7a98ead6d).html.
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Rat neuronal nitric oxide synthase (nNOS) is a flavo-hemoprotein that catalyses the NADPH and O2-dependent conversion of L-arginine (L-arg) to L-citrulline and nitric oxide (NO) via the intermediate N-hydroxyarginine. nNOS is a homodimer, where the subunits are modular and are comprised of an N-terminal oxygenase domain (nNOSoxy) that binds iron protoporphyrin IX (heme), (6R)-5,6,7,8-tetrahydro-biopterin (H4B) and L-arg, and a C-terminal flavoprotein or reductase domain (nNOSred) that binds NADPH, FAD and FMN. Regulation of NO biosynthesis by nNOS is primarily through control of interdomain electron transfer processes in NOS catalysis. The interdomain electrons transferred from the FMN to the heme domain are essential in the delivery of electrons required for O2 activation (which occurs in the heme domain) and the subsequent NO synthesis by NOS. Both spectroscopic and kinetic approaches have been used in studying the nature and control of interdomain electron transfer, reaction mechanism and structural changes during catalysis in WT and R1400E nNOS in both full length (FL) and nNOSred. Cytochrome c reduction activity of nNOS was used to determine kinetic parameters for NADPH for FL and nNOSred, WT and R1400E nNOS in the presence and absence of calmodulin (CaM). FL nNOS, where both domains (nNOSred and nNOSoxy) were present, was proven to be more stable and more catalytically efficient than nNOSred by itself. Additionally it was observed that R1400E is still promoting electron transfer despite being thought to lower the affinity of the enzyme to the substrate (NADPH); R1400E also showed lower catalytic efficiency and lower dependence on CaM/Ca2+ compared to the WT. The structure of the functional output state has not yet been determined. In the absence of crystallographic structural data for the NOS holoenzyme, it was important to experimentally determine conformational changes and distances between domains in nNOS. A pulsed EPR spectroscopy (PELDOR) approach has been utilised to gain important and unique information about the conformational energy landscape changes in nNOS. In the presence of CaM, PELDOR results for FL WT nNOS shows a complex energy landscape with multiple conformational states, while in the absence of CaM the interflavin distance distribution matches that exhibited by nNOSred CaM- in the presence of NADP+, suggesting that CaM binding affects some major large-scale conformational changes which are involved in internal electron transfer control in nNOS. A high-pressure stopped-flow technique was also used to perturb an equilibrium distribution of conformational states, to observe the effect of the pressure on the internal electron transfer and to study the kinetics of NADPH oxidation, flavin reduction by NADPH and NO formation. It was shown that high pressure is forcing major changes in the conformational energy landscape of the protein, affecting internal electron transfer. NO formation studies under pressure show that the R1400E mutation in FL nNOS may be affecting protein/NADPH affinity and flavin reduction, but it has no effect on the heme reduction step.
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Nardi, Geisson Marcos. "Óxido nitrico proveniente da isoforma neuronal da enzima óxido nítrico sintase (NOS-1)." Florianópolis, SC, 2011. http://repositorio.ufsc.br/xmlui/handle/123456789/95541.
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Tese (doutorado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas, Programa de Pós-Graduação em Farmacologia, Florianópolis, 2011Made available in DSpace on 2012-10-26T03:11:53Z (GMT). No. of bitstreams: 1 295312.pdf: 1743921 bytes, checksum: 5721b330602424fbe65211dfbf890383 (MD5)
Vários estudos demonstraram que produção excessiva de NO, relacionada com o aumento da expressão da NOS-2, contribui para as alterações hemodinâmicas observadas durante a sepse. No entanto, alguns trabalhos mostram que a inibição desta enzima não reverte a hipotensão, a hiporeatividade a agentes vasoconstritores e não influencia na sobrevivência de animais sépticos. Portanto, resolvemos investigar o papel do NO proveniente da isoforma neuronal da óxido nítrico sintase (NOS-1) sobre a reatividade a agentes vasoconstritores, e sua influência na progressão da sepse bem como o efeito de agonistas opióides sobre parâmetros comumente avaliados nesta doença. Nossos resultados demonstram que animais sépticos são sensíveis a analgesia com drogas opióides em modelo de dor por estímulo térmico e, além disso, os analgésicos opióides reduziram a hipotensão e hiporeatividade vascular induzidas pela sepse. Estes compostos quando administrados em doses baixas não interferiram na sobrevivência de animais sépticos, enquanto que doses maiores aumentam a mortalidade. A inibição da NOS-1 melhorou a reatividade vascular a agonistas e -adrenérgicos, tanto na fase inicial quanto na fase tardia da sepse. Tanto a NOS-1 quanto a guanilato ciclase solúvel tem sua expressão aumentada nas camadas de músculo liso vascular da aorta e do leito vascular mesentérico, e nos momentos mais tardios, ambas as enzimas interagem fisicamente no leito vascular mesentérico. Parte do mecanismo de reversão da hiporeatividade a agonistas -adrenérgicos, após inibição da NOS-1, se deve a redução na formação de GMPc. No entanto, a reversão da hiporeatividade vascular a agentes -adrenérgicos durante a sepse pelo 7-NI parece ser independente do aumento nos níveis de cAMP. As alterações promovidas pelo NO proveniente da NOS-1 no início da sepse estão relacionadas com a instalação da hipotensão, disfunção vascular, alterações na glicemia e nos níveis de leucócitos sanguíneos. A redução do conteúdo enzimático da NOS-1, reduz ou abole as alterações patológicas induzidas pela sepse. Nosso trabalho demonstra que o NO proveniente da NOS-1 participa ativamente na disfunção vascular promovida pela sepse.
Several studies have shown that overproduction of NO, associated with the increased expression of NOS-2, contributes to the hemodynamic changes observed in sepsis. However, inhibition of NOS-2 does not reverse hypotension, hyporesponsiveness to vasoconstrictor and does not influence the survival of septic animals. Therefore, we decided to investigate the role of NO derived from the neuronal isoform of nitric oxide synthase (NOS-1) on the reactivity to vasopressor agents and the progression of sepsis as well as the effect of opioid agonists on parameters commonly evaluated in this pathology. Our results demonstrate that septic animals are sensitive to analgesia with opioids in the pain model of thermal stimulation. In addition, opioids reduced the hypotension and vascular hyporesponsiveness induced by sepsis. When administered in low doses these drugs did not affect the survival of septic animals, whereas higher doses increased the mortality. The inhibition of NOS-1 improved the vascular reactivity to and -adrenergic agonists, both in early and late phase of sepsis. The expression of NOS-1 and soluble guanylate cyclase was increased in vascular smooth muscle layers of aorta and mesenteric vascular bed and both enzymes interact physically in the mesenteric vascular bed in late phase of sepsis. At least part of the mechanism of the recovery in the responsiveness to adrenergic agonists, after inhibition of NOS-1, is due to the reduced formation of cGMP. The changes promoted by NOS-1-derived NO in early sepsis are associated with the onset of hypotension, vascular dysfunction and changes in blood glucose levels and blood leukocytes. The reduction in the NOS-1 enzyme content reduces or abolishes the pathological changes induced by sepsis. Our work demonstrates that NOS-1-derived NO plays a role in promoting vascular dysfunction in sepsis.
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Coelho, Camila Henriques. "Análise da inibição da óxido nítrico sintase neuronal (nNOS) na liberação de vasopressina durante sepse experimental." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-30102009-022744/.
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A fisiopatologia da sepse se caracteriza por hipotensão acompanhada de aumento da secreção de vasopressina (AVP) na fase inicial e diminuição numa fase mais tardia. Essa hipotensão é em parte devido ao aumento da quantidade de óxido nítrico, que juntamente com outros mediadores tem sua produção aumentada durante a sepse. A óxido nítrico sintase (NOS) é responsável pela síntese deste mediador, e sua isoforma neuronal (nNOS) está presente no músculo esquelético, pulmões, testículos, próstata, pele e também nos neurônios vasopressinérgicos do hipotálamo. O presente trabalho avaliou a participação do óxido nítrico produzido pela isoforma neuronal de NOS sobre a secreção temporal de AVP durante a sepse experimental. Ratos Wistar receberam injeção i.p. de 7-nitroindazol (50mg/kg ou 80mg/kg), inibidor específico da NOS neuronal, ou DMSO 10% + óleo de gergelim na proporção 1:9 (veículo) e após 30 minutos foram submetidos ao estímulo séptico por ligadura e perfuração cecal (CLP) ou à operação fictícia (OF). Em um grupo de animais, a sobrevida foi avaliada durante 5 dias. Em outro grupo, os animais foram decapitados 0, 4, 6, 18 e 24 horas após a cirurgia e o sangue processado para determinação do hematócrito, sódio sérico, osmolalidade, proteínas, glicose, creatinina, nitrato sérico e AVP plasmática. A neurohipófise foi removida para a determinação do conteúdo de AVP, e o hipotálamo dissecado para a determinação da atividade da NOS total. A mortalidade observada após CLP não foi modificada com o pré-tratamento com 7-NI (50mg/kg), assim como os aumentos temporais de hematócrito, glicose e nitrato sérico observados. As proteínas plasmáticas e o sódio sérico apresentaram diminuição após CLP e o pré-tratamento com 7-NI antecipou a perda proteica e postergou a diminuição do sódio sérico. Os animais após CLP não apresentaram alterações de creatinina e osmolalidade, entretanto quando prétratados com 7-NI, apresentaram aumento em 6 e 18 horas e diminuição a partir de 4hs, respectivamente. A atividade da NOS total no hipotálamo aumentou nos tempos determinados de 4 e 24 horas após CLP e este aumento foi reduzido com o prétratamento com o 7-NI nas doses de 50 e 80mg/kg, respectivamente. O conteúdo neurohipofisário de AVP diminuiu em 4, 6 e 18 horas após CLP e o pré-tratamento com 7-NI reduziu os estoques apenas em 0 e 6 horas. As concentrações plasmáticas de vasopressina apresentaram-se aumentadas sómente 6 horas após CLP e o pré-tratamento não alterou essas concentrações. Esses resultados permitem concluir que o NO produzido pela NOS neuronal não teria uma tarefa substancial na secreção de vasopressina durante sepse experimental.The pathophysiology of sepsis is caracterized by hypotension accompanied by increase of vasopressin secretion (AVP) in early phase and decrease during late phase. This hypotension is due, in part, to the increase of nitric oxide (NO) production, that, like other mediators, shows high production during sepsis. Nitric oxide synthase (NOS) is responsible by synthesis of NO. The neuronal isoform of NOS is present in skeletic muscle, testicles, prostate, skin and vasopressinergics neurons of hypothalamus. The present work evaluated the participation of nitric oxide produced by neuronal NOS in temporal vasopressin secretion during experimental sepsis. Rats Wistar received intraperitoneal injection of 7-nitroindazole (50 or 80 mg/kg), an inhibitor of neuronal nitric oxide synthase activity, or DMSO 10% + sesame oil in the proportion 1:9 (vehicle) and after 30 minutes, they were submited to septic stimulus by cecal ligation and puncture (CLP) or to sham operation. In one of the groups, the survival rate was evaluated during 5 days. In other group, the animals were decapited 0, 4, 6, 18 and 24 hours after CLP and the blood was processed to determinate haematocrit, serum sodium, osmolality, proteins, glucose, creatinine, serum nitrate, and plasma AVP. Neurohypophysis was removed to determination of vasopressin content, and hypotalamus was dissected to determinate total NOS activity. Mortality observed after CLP was not affected by periferal injection of 7-nitroindazole (50 mg/kg) as well as haematocrit, glucose and nitrate increase. Serum sodium and plasma protein decreased after CLP and the treatment antecipated the loss protein, and delayed serum sodium decrease. CLP animals didn\'t show creatinine and osmolality alterations, but when treated with 7-nitroindazole, showed increase 6 and 18 hours, and decrease 4 hours, respectively. NOS activity in hypothalamus increased 4 and 24 hours after CLP, and was reduced with 7-NI pretreatment (50 and 80 mg/kg respectively). AVP neurohypophysis content diminished 4, 6 and 18 hours after CLP and 7-NI reduced the content just at 0 and 6 hours. Vasopressin plasma concentration increased just 6 hours after CLP and 7-NI pretreatment didn\'t alter this parameter. We concluded that NO produced by neuronal NOS doesn\'t have a substantial role in vasopressin secretion during experimental sepsis.
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Kirsten, Gabriela Pena Chaves. "O receptor canabinóide CB1 nos núcleos da base e a sua participação no processo degenerativo em modelos da Doença de Parkinson." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-20092013-093533/.
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Os receptores canabinóides CB1 são abundantemente expressos nos núcleos da base (NB), sugerindo a participação do sistema canabinóide na Doença de Parkinson (DP). Os objetivos deste estudo foram investigar a localização do CB1 nos NB de ratos; avaliar o decurso temporal de sua expressão e de marcadores neuronais em modelo experimental da DP in vivo, e avaliar os efeitos do tratamento com compostos canabinóides em modelos experimentais da DP in vivo e in vitro. Nossos resultados mostraram que o CB1 é predominantemente expresso em neurônios GABAérgicos nos NB. A lesão dopaminérgica produziu mudanças temporais distintas da expressão do CB1 nas estruturas dos NB. O tratamento com o agonista canabinóide ACEA agravou à lesão dopaminérgica e o desempenho comportamental motor. Por outro lado, o tratamento com o antagonista AM 251, embora não tenha gerado diferenças neuroquímicas, gerou melhoras nos testes comportamentais. Por fim, em nosso modelo in vitro, o tratamento com inibidor de recaptação da anandamida AM 404 gerou uma discreta redução dos níveis de morte celular.Cannabinoid receptors CB1 are abundantly expressed in the basal ganglia (BG), suggesting the involvement of the cannabinoid system in Parkinson\'s disease (PD). The objectives of this study were to investigate the location of CB1 in BG of rats; evaluate the time course expression of CB1 and neuronal markers in an experimental model of PD in vivo, and evaluate the effects of treatment with cannabinoids compounds in experimental models of PD in vivo and in vitro. Our results showed that CB1 is predominantly expressed in GABAergic neurons in BG. The dopamine lesion produced distinct temporal changes in the expression of CB1 in BG structures. Treatment with the cannabinoid agonist ACEA aggravated the dopaminergic lesion and the motor behavioral performance. Moreover, the treatment with the antagonist AM 251, although have not generated neurochemical changes,it promoted improvements in behavioral tests. Finally, in our in vitro model, the treatment with Anandamide transport inhibitor AM 404 led to a slight reduction in the levels of cell death.
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Mari, Renata de Britto. "Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-10082010-160611/.
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Os últimos anos se caracterizaram pelo aumento significativo da população idosa mundial. Por esta razão, a preocupação com o idoso está se tornando uma constante em nossa sociedade, uma vez que o envelhecimento resulta em comprometimento das funções fisiológicas, acompanhado ou não de alterações estruturais. No trato gastrointestinal (TGI), o processo de envelhecimento pode provocar alterações morfofuncionais significativas. A regulação da motilidade do TGI é controlada principalmente pelos neurônios mioentéricos do sistema nervoso entérico. A diminuição na densidade destes neurônios no cólon pode levar à redução na frequência e na amplitude da contração colônica manifestada como constipação. As ações que visam diminuir os efeitos do envelhecimento no TGI incluem aquelas relacionadas à dieta alimentar, entre as quais se destaca a restrição calórica. A restrição calórica, além de apresentar efeito protetor nos neurônios mioentéricos durante o envelhecimento, também é responsável pela diminuição da morte neuronal por apoptose, processo este acentuado com o envelhecimento. Assim sendo, este trabalho teve por objetivo avaliar os efeitos de diferentes níveis de restrição calórica sobre a plasticidade dos neurônios mioentéricos NADPH e acetilcolinesterase positivos do cólon de ratos Wistar durante o processo de envelhecimento por meio das análises ultraestrutural (microscopia eletrônica de transmissão) e morfoquantitativa. Para tanto foram utilizados 40 ratos machos (Rattus norvegicus), da linhagem Wistar, distribuídos em quatro grupos (n= 10/grupo): CI- animais de seis meses; SR- animais de 18 meses alimentados com dieta normal; RCI- animais de 18 meses alimentados com dieta com 12% de restrição calórica; RCII- animais de 18 meses submetidos à restrição calórica de 30%. Aos seis meses de idade, os animais foram transferidos para o biotério setorial, onde permaneceram até aos 18 meses sob condições ambientais controladas de temperatura e de iluminação e água ad libitum. Foi possível observar que a RC em nível de 30% minimizou de forma eficaz os efeitos deletérios do envelhecimento nos neurônios mioentéricos, podendo ser adotada como alternativa contra os distúrbios gastrointestinais comuns em indivíduos idosos.The last years were characterized by a significant increase in the elderly population. For this reason, concern for the elderly is becoming a constant in our society, since the aging results in impairment of bodily function, or not accompanied by structural changes. In the gastrointestinal tract (GI), the aging process can cause significant morphological changes. The regulation of motility of the gut is controlled mainly by myenteric neurons of the enteric nervous system. The decrease in the density of neurons in the colon can lead to a reduction in the frequency and amplitude of contraction expressed as colonic constipation. The actions aimed at reducing the effects of aging on the GI system include those related to diet, among which stands out caloric restriction. Caloric restriction, and have a protective effect on the myenteric neurons during aging, is also responsible for the decrease of neuronal death by apoptosis, a process accentuated with aging. Thus, this study was to evaluate the effects of different levels of calorie restriction on the plasticity of myenteric neurons NADPH and acetylcholinesterase positive of the colon of rats during the aging process by means of ultrastructural (transmission electron microscopy) and morphoquantitative analysis. Therefore, we used 40 male Wistar rats (Rattus norvegicus), divided into four groups (n = 10): CI- animals six months; SR- animals 18 month fed a normal diet; RCI - animals 18 months fed a diet with 12% caloric restriction; RCII- animals 18 months fed a diet with 30% caloric restriction. At six months, the animals were transferred to the vivarium sector, where they remained up to 18 months under controlled conditions of temperature and light and water ad libitum. It was observed that the RC level of 30% effectively minimized the deleterious effects of aging on myenteric neurons, which may be adopted as an alternative against the common gastrointestinal disorders in the elderly.
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Hajj, Glaucia Noeli Maroso. "A proteína prion celular e seus ligantes-vitronectina, STI1 e laminina - nos mecanismos de plasticidade neuronal." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-21122015-165320/.
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Prions são agentes etiológicos das encefalopatias espongiformes transmissíveis, doenças que acometem tanto homens quanto animais. A proteína infecciosa, PrPsc, é uma isoforma de uma proteína celular normal denominada PrPc. As funções de PrPc ainda causam controvérsia na literatura, mas já foi demonstrada a participação de PrPc em uma variedade de fenômenos biológicos, como homeostase de íons cobre, proteção contra estresse oxidativo, sinalização celular e neuritogênese entre outros. A interação de PrPc com laminina, uma proteína de matriz extracelular, leva a formação e manutenção de neuritos em neurônios hipocampais. Seguindo este caminho, demonstramos no presente trabalho a interação de PrPc com outra proteína de matriz extracelular, vitronectina (Vn). Esta interação também leva ao crescimento neurítico, tanto em células do sistema nervoso central quanto do sistema nervoso periférico. No sistema nervoso periférico, a ausência de PrPc é compensada por integrinas, no fenômeno da neuritogênese. Relatamos também que a interação de PrPc com STI1, uma cochaperonina, leva tanto a neuritogênese quanto a neuroproteção por vias de sinalização distintas. A ligação de PrPc com Vn e STI1 se dá através de domínios contíguos, de modo que as interações são excludentes sendo aquela com Vn mais favorável, como observado em ensaios de ligação in vitro, quanto através do fenômeno de neuritogênese. Já a ligação de laminina se dá em um domínio distante daqueles de ligação à Vn e STI1. Assim, pode ser observada cooperatividade entre laminina e STI1 no fenômeno da neuritogênese. Por fim, demonstra-se que a interação PrPc-laminina in vivo é importante para os mecanismos de consolidação da memória.Prions are involved in numerous neurodegenerative diseases in humans and animals called transmissible spongiform encephalopathies. PrPsc, the infectious protein, is an isoform of a normal cellular protein named PrPc. PrPc functions are still under debate, among them Cu++ homeostase, protection against oxidative stress, cell survival signaling and neuritogenesis. PrPc interaction with laminin (Ln), an extracellular matrix protein, leads to neurite growth and maintenance. PrPc interaction with another extracellular matrix protein, vitronectin (Vn) is here demonstrated. This association leads to neurite growth in hippocampal and dorsal root ganglia cells. In dorsal root ganglia cells, PrPc ablation can be compensated by integrins, at least in the neuritogenesis phenomenon. PrPc is also a cellular ligand for STI1, a co-chaperone, mediating neuritogenesis or neuroprotection, depending on the activated cell signaling pathway. Vn and STI1 binding sites at the PrPc molecule are localized in contiguous domains what makes their binding to PrPc mutually exclusive. The first is more favorable, as observed in vitro and ex vivo. On the other hand, Ln binding site at PrPc is confined to a domain distinct from those where Vn or STI1 associate. Furthermore, laminin and STI1 have additive effects on neurite outgrowth. The importance of PrPc-Ln interaction is also observed in vivo, since the complex participates in memory consolidation mechanisms.
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Carvalho, Altiere Araujo. "Estudo da plasticidade cruzada nos centros de fala e audição em pessoas ouvintes e surdas através de psicofísica e ressonância magnética funcional." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-26112009-151337/.
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O dito popular afirma que quando uma pessoa perde um dos sentidos há uma compensação por parte dos outros sentidos para suprir a perda. Através de três experimentos psicofísicos baseados no modelo de Posner (Inibição de Retorno) e técnicas de Ressonância Magnética Funcional, surdos congênitos foram comparados a pessoas ouvintes com o objetivo de verificar se os surdos possuem processos atencionais diferentes dos ouvintes, e se as mesmas áreas corticais como a área de Wernicke, Broca e Córtex auditivo - eram ativadas em ambos os grupos. A tarefa consistia em pressionar um botão todas as vezes que os sujeitos detectassem a presença de um quadrado maior (alvo) apresentado em uma tela, enquanto também eram apresentados quadrados menores (pista) ora do mesmo lado, ora do lado oposto ao alvo. Através do Experimento I se pôde verificar que ambos os grupos apresentaram os fenômenos clássicos do Paradigma de Posner: Facilitação ou Inibição de Retorno, o que denotou a possibilidade de mecanismos atencionais semelhantes para ambos os grupos. Foi observado, porém, que os ouvintes eram mais rápidos que os surdos para responder à tarefa quando o intervalo temporal entre pista e alvo era longo (800ms), comparado ao tempo que levavam para responder quando o intervalo entre pista e alvo era curto (100 ms). O Experimento I suscitou a hipótese de que os surdos possivelmente apresentassem uma diferença de processamento temporal. No Experimento I todas as condições eram apresentadas de forma randômica. O Experimento II foi elaborado com o objetivo de por em evidência a 22 diferença dos TRM para intervalos curtos e longos, portanto os intervalos entre pista e alvo passaram a ser apresentados de forma fixa. Ao comparar os resultados do Experimento I com os do Experimento II (Intervalos Temporais Fixos), se pode verificar que os ouvintes apresentaram Tempos de Reação Manual mais lentos, enquanto os surdos apresentaram as mesmas médias a despeito da vantagem temporal, o que levou a sugerir a hipótese de que os surdos apresentem um déficit no processamento temporal. O experimento III consistiu na utilização do Paradigma de Posner enquanto os sujeitos eram submetidos ao exame de Ressonância Magnética Funcional com o objetivo de investigar se as regiões corticais ativadas poderiam ser semelhantes nos dois grupos. As imagens por Ressonância Magnética Funcional (RMF) demonstraram ativações nas áreas de Wernickie, Broca, e córtex auditivo em ambos os grupos enquanto executavam a tarefa, que embora não possuísse nenhum contexto semântico explícito, possuía o tempo como o principal parâmetro físico no qual os sujeitos pudessem se basear para melhorar o desempenho na tarefa. O tempo é um dos parâmetros físicos primários da língua oral, diferente da língua de sinais que possui o parâmetro visual e espacial como primário. Os resultados sugerem que as ativações corticais nos centros de audição e fala podem indicar uma plasticidade cruzada no grupo de surdos. Ainda, a participação do córtex auditivo no processamento da elaboração de estratégias para responder a uma tarefa que não contenha um contexto semântico explicito possivelmente indica sua participação no processamento de linguagem.It is popularly said that when a person loses one sense, there is a compensation by the other remaining senses to suppress the loss. Throughout three Phsycophysic Experiments based on Inhibition of Return Posners Paradigm and Functional Magnetic Resonance (fMRI) Techniques, congenital deaf people were compared to normal hearing people in order to check if deaf people possess different attentional pattern compared to normal hearing people, and if the same cortical areas Wernicke and Brocas area and Hearing Cortex were activated in both groups. Experiment I consisted on pressing a button every time the presence of a big square (target) was detected by subjects while non-predictive small squares (cue) were also presented at the same or opposite side of the target. At Experiment I it was observed that both groups presented Posners Paradigm classical phenomena: Facilitation or Inhibition of Return, what suggested the possibility that attentional pattern may be similar to both groups. Therefore, it was observed that normal hearing people were faster than deaf people to respond to the task when time interval between cue and target was long (800 ms) when compared to the time they spent to respond when time interval between cue and target as short (100 ms). 24 Experiment I raised the hypotheses that possibly deaf people may present a temporal processing difference. At Experiment I every condition was randomly presented. Experiment II was elaborated to highlight MRT differences between short and long time intervals, so every time interval was presented on a fixed order. Comparison of Experiment I and II (Fixed Time Intervals) showed that normal hearing people presented shorter Manual Reaction Times (MRT), while deaf people kept the same averages despite the temporal advantage, what suggested that deaf people may present a deficit on temporal processing. Experiment III used Posners Paradigm while subjects were submitted to fMRI scanning in order to check if activated cortical regions could be similar in both groups. fMRI images demonstrate Wernicke and Brocas area and hearing cortex activations in both groups while executing the task, which, although did not have any explicit semantic content, had time as the main physical parameter on which subjects could be based to increase performance to respond to the task. Time is one of the oral language primary physical parameter, different of signed language which has visual and spatial parameters as primaries. Results suggest that cortical audition center activations may indicate a cross-modal plasticity at the deaf group. Yet, participation of hearing cortex on strategy elaboration to respond to a task which does not have any explicit semantic content possibly indicates the participation of hearing cortex on language processing.
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Candemir, Esin [Verfasser], and Andreas [Gutachter] Reif. "Involvement of neuronal nitric oxide synthase (NOS-I) PDZ interactions in neuropsychiatric disorders / Esin Candemir ; Gutachter: Andreas Reif." Würzburg : Universität Würzburg, 2018. http://d-nb.info/1162444371/34.
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Tajouri, Lotfi, and n/a. "Gene Expression Analysis and Genetic Studies in Multiple Sclerosis." Griffith University. School of Health Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060111.123933.
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Multiple Sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS). As part of this disorder the myelin sheath undergoes degeneration, leading to alterations in the conductivity of axons, and impaired function. The onset of the disease occurs in young adults and clinical pathology is characterised by varying severity. These include i) Relapsing Remitting MS (RR-MS), ii) Secondary Progressive MS (SP-MS) and iii) Primary Progressive MS (PP-MS). MS is more prevalent in women and accounts for more than two thirds of all MS sufferers. MS is considered to be a multifactorial disorder with both genetic and environmental components. The prevalence of MS is dependent on geographical localisation, with lower sunlight exposure linked to higher prevalence. Also, studies show an increased risk in close relatives, or in identical twins, indicating a significant genetic component to the disorder. There are a number of genes that may plausibly be involved in MS pathophysiology. These include myelin-related genes, such as the myelin basic protein (MBP), immune-related genes, such FC receptor and osteopontin, and heat shock proteins such as xb crystallin. These candidate genes have been implicated in a variety of ways but usually through immunological and/or genetic studies. One of the most consistent findings in recent years has been the association of disease with alterations in the specific major histocompatibility complex (MHC) localised to chromosome 6p21.3, and includes MHC I, II, III. Genome wide screens have permitted the identification of loci in the genome, which are associated with MS susceptibility. The number of genes involved in MS is unknown and several case-control association studies have been undertaken to reveal the involvement of potential candidate genes. In general terms, current research is aimed at determining allelic variation of candidate genes. Such genes have been implicated in MS because they reside within susceptible regions of the chromosome associated with MS or they have a plausible potential pathophysiological role in MS. Candidate loci investigated in this study, for association with MS susceptibility, include members of the nitric oxide synthase family of metabolic proteins (inducible NOS, iNOS/NOS2A and neuronal NOS, nNOS), methylenetetrahydrofolate reductase (MTHFR), catechol-O-methyl transferase (COMT), and vitamin D receptor (VDR). The MS population used in all studies consisted of over 100 MS cases and gender, age and ethnicity matched controls. In our study of inducible and neuronal NOS genes, PCR based assays were developed to amplify a region of both promoters that contained known microsatellite variation. Supporting phyisological data suggests that the neuroinflammatory aspects of MS are associated with aberrant NO production, which may be due to aberrant regulation of NOS activity. Specific amplified products were identified by fluorescent capillary electrophoresis and allele frequencies were statistically compared using chi-squared analysis. In the nNOS and iNOS study, no association was identified with allele frequency variation and MS susceptibility (nNOS: ?2=5.63, P=0.962; iNOS: ?2=3.4; P=0.082). Similarly, no differences in allele frequencies were observed for gender or clinical course for both markers (Pvalue greater than 0.05). In short, results from this study indicate that the NOS promoter variations studied do not play a significant role in determining susceptibility to MS in the tested population. The COMT and MTHFR genes are localised at 22q12-13 and 1p36.3 respectively, regions of the genome that have been found to be positively associated with MS susceptibility. In our research, we set out to examine the G158A change in the 4th exon of the COMT gene. This functional mutation leads to an amino acid change (valine to methionine) that is directly associated with changes in the activity of COMT. The MTHFR enzyme plays a role in folate metabolism, and can be implicated in the turnover of homocysteine. Previous investigations have shown that high levels of homocysteine are encountered in MS patients, where it is also linked to demyelination in the CNS. In our study the aim was to examine the C677T variation (alanine to valine amino acid change) in the exon 4 coding region of the MTHFR gene and the G158A variation in the COMT gene. Restriction fragment length polymorphism (RFLP) analysis and gel electrophoresis was used to identify specific alleles for both COMT and MTHFR. However, as with the NOS study, no specific association was identified between MS susceptibility and variation for either of the tested COMT or MTHFR (Pvalue greater than 0.05) variants. In a final genomic investigation of the MS population, three variations in the VDR gene were analysed for association with MS susceptibility and pathology. Using RFLP analysis, three VDR variants were investigated with genotypes detected using the Taq I, Apa I and Fok I restriction enzymes. In contrast to previous genotypic analyses, this study did show a positive association, specifically between the functional variation in exon 9 of the VDR gene and MS (Taq I, 2= 7.22, P= 0.0072). Interestingly, the Apa I variant of VDR was also found to be associated with MS ( 2=4.2, P=0.04). The Taq I and Apa I variants were also found to be in very strong and significant linkage disequilibrium (D'=0.96, Pvalue less than 0.0001) and their associations were more prominent with the progressive forms of MS (SP-MS and PP-MS). In addition to genotypic analysis of a clinical population, additional research was undertaken to identify novel targets for MS susceptibility studies. Global gene expression analysis was undertaken using comparative subtractive fluorescent microarray technology to examine differences in gene activity (expression) in age and sex matched MS plaque tissue and anatomically matched normal white matter (NWM). MS plaques were obtained post mortem from MS sufferers with no drug history in the last two months before death and matched anatomically to healthy white matter from donors with no previous neurological disorders. Target arrays consisted of 5000 cDNAs and analysis was conducted using the Affymetrix 428 scanner. In this way, 139 genes were shown to be differentially regulated in MS plaque tissue compared to NWM. Of these, 69 genes showed a common pattern of expression in the chronic active and acute plaque tissues investigated (Pvalue less than 0.0001, a=0.73); while 70 transcripts were uniquely differentially expressed ( 1.5-fold) in either acute or chronic active lesions. To validate the gene expression profile results, quantitative real time reverse transcriptase (RT) PCR (Q-PCR) analysis was performed. 12 genes were selected because they were shown to be differentially expressed by array analysis in this study, or because of their involvement in MS pathology. These included transferrin (TF), superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPX1), glutathione S-transferase pi (GSTP1), crystallin, alpha-B (CRYAB), phosphomannomutase 1 (PMM1), tubulin beta-5 (TBB5), inositol 1,4,5-trisphosphate 3-kinase B (ITPKB), calpain 1 (CAPNS1), osteopontin (SPP1 or OPN), as well as the signal transducer and activator of transcription 1 (STAT1) and protein inhibitor of activated STAT1 (PIAS1). Both absolute (copy number) and comparative differences in the relative levels of expression in MS lesions and NWM were determined for each gene. The results from this study revealed a significant correlation of real time PCR results with the microarray data, while a significant correlation was also found between comparative and absolute determinations of fold. As with the results of array analysis, a significant difference in gene expression patterning was identified between chronic active and acute plaque pathologies. For example, a up to 50-fold increase in SPP1 and ITPKB levels in acute plaques contrasted with the 5-fold or less increase in chronic active plaques (P less than 0.0.1, unpaired t-Test). Of particular note, gamma-amino butyric acid receptor ?2 (GABG2), integrin ?5 (ITGB5), complement component 4B (C4B), parathyroid hormone receptor 1 (PTHR1) were found up-regulated in MS and glial derived neurotropic factor ?2 (GDNFA2), insulin receptor (INSR), thyroid hormone receptor ZAKI4 (ZAKI4) were found down-regulated in MS. Data also revealed a decreased expression of the immune related genes STAT1 and PIAS1 in acute plaques. In conclusion, this research used both genomic analysis and technologies in gene expression to investigate both known and novel markers of MS pathology and susceptibility. The study developed tools that may be used for further investigation of clinical pathology in MS and have provided interesting initial expression data to further investigate the genes that play a role in MS development and progression.
Books on the topic "Neuronal NOS"
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Thomas, Schiex, ed. Intelligence artificielle et informatique théorique. Toulouse: Cépaduès-éd., 1994.
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Baldi, Elisabetta, and Corrado Bucherelli. Neuroscience. Florence: Firenze University Press, 2017. http://dx.doi.org/10.36253/978-88-6453-638-5.
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This bibliographic material is patrimony of our Laboratory of the Behavior Physiology. This research unit originated in 1972 by will of Aldo Giachetti (until 1990) and with the beginning of the activity of Corrado Bucherelli. In the early 1980s, with Carlo Ambrogi Lorenzini (until 2004), the cataloging became more capillary and systematic, to continue to this day. All the researchers who worked in our laboratory contributed to this collection (Giovanna Tassoni 1986-2000, Benedetto Sacchetti 1996-2002 and Elisabetta Baldi from 1991). The study of learning, memory and behavior requires to follow a broad spectrum of neuroscience topics, ranging from neuronal biochemistry to neuropsychology. The Authors’ idea of publishing this collection comes from believing that a such website, though not exhaustive, might be a useful and targeted tool for the selection of bibliographic material in the field of behavioral neuroscience. The bibliographic references present at the publication (29500), accompanied by a brief comment highlighting the contents, are organized in relation to the topics (represented by the 99 themes) constituting the publication itself. The intersection of several references will point out the topics that represent them simultaneously. Concerning neurotransmitters and neuromodulators, references to agonists, antagonists or molecules interfering with the activity of these synapses have been inserted in the pages of the implicated neurotransmitter (e.g. acetylcholine). The pages including topics that could have been dealt with separately (e.g. active and passive avoidance) are introduced by a short explanatory note. The comment of each publication highlights the animal species used. Each comment is intended to indicate the content rather than the experimental results of paper. This choice comes from wanting to provide the reader with a more objective and less speculative comment.
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Montgomery, Erwin B. Controlling the Flow of Electrical Charges. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0004.
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In depolarization to effect neuronal activations,, electrical charges are delivered to the neuron to affect the electrical potential across the neuronal membrane to subsequently affect voltage-gated ionic conductance channels. The orientation of the field of electrical charges to the neuronal membrane is critical. Electrical charges flow from the negative contact to the positive contact. The negative electrostatic charge “pushes” negative charges onto the outer surface of the neuron, which results in depolarization of the neuronal membrane. Neurons near the positive contact will not have negative electrical charges deposited on the outer surface, will not be depolarized, and thus, are not activated. Likewise, neurons whose membranes are oriented parallel to the lines of electrical forces that move electrical charges will not receive the electrical charges and, consequently, will not be activated. The electronics of the DBS systems are designed to control the electrostatic forces so as to control the activations of the nervous system to generate benefit and avoid adverse effects.
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Soffietti, Riccardo, Hugues Duffau, Glenn Bauman, and David Walker. Neuronal and mixed neuronal–glial tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0008.
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Neuronal and mixed neuronal-glial tumours are rare tumours of the central nervous system that occur more commonly in children. Despite a generally benign course, most tumours cause medically intractable seizures, and have been denominated as ‘long-term epilepsy-associated tumours’. The World Health Organization classification distinguishes nine histological variants: dysplastic gangliocytoma of the cerebellum/Lhermitte–Duclos disease, desmoplastic infantile astrocytoma and ganglioglioma, dysembryoplastic neuroepithelial tumour, gangliocytoma and ganglioglioma, central neurocytoma and extraventricular neurocytoma, cerebellar liponeurocytoma, papillary glioneuronal tumour, rosette-forming glioneuronal tumour of the fourth ventricle, and spinal paraganglioma. Early surgery with complete resection may significantly improve the likelihood of postoperative epilepsy freedom. Conformal radiotherapy can be considered in case of patients with incompletely resected symptomatic tumours, atypical or high-grade tumours, or in the case of multiple recurrences despite resections. The role of chemotherapy in these lesions remains poorly defined, while targeted therapies are now available to impact some molecular alterations.
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Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.
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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.
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Nieder, Andreas. Neuronal Correlates of Non-verbal Numerical Competence in Primates. Edited by Roi Cohen Kadosh and Ann Dowker. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199642342.013.027.
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Non-verbal numerical competence, such as the estimation of set size, is rooted in biological primitives that can also be explored in animals. Over the past years, the anatomical substrates and neuronal mechanisms of numerical cognition in primates have been unravelled down to the level of single neurons. Studies with behaviourally-trained monkeys have identified a parietofrontal network of individual neurons selectively tuned to the number of items (cardinal aspect) or the rank of items in a sequence (ordinal aspect). The properties of these neurons’ numerosity tuning curves can explain fundamental psychophysical phenomena, such as the numerical distance and size effect. Functionally overlapping groups of parietal neurons represent not only numerable-discrete quantity (numerosity), but also innumerable-continuous quantity (extent) and relations between quantities (proportions), supporting the idea of a generalized magnitude system in the brain. Moreover, many neurons in the prefrontal cortex establish semantic associations between signs and abstract numerical categories, a neuronal precursor mechanisms that may ultimately give rise to symbolic number processing in humans. These studies establish putative homologies between the monkey and human brain, and demonstrate the suitability of non-human primates as model system to explore the neurobiological roots of the brain’s non-verbal quantification system, which may constitute the phylogenetic and ontogenetic foundation of all further, more elaborate numerical skills in humans.
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DeFelipe, Javier. Cajal's Neuronal Forest. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190842833.001.0001.
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Cajal’s Neuronal Forest: Science and Art continues the tradition set forth in the 2009 publication Cajal’s Butterflies of the Soul: Science and Art. This new compilation contains a vastly large collection of beautiful figures produced throughout the nineteenth century and the beginning of the twentieth century. These images continue to represent and illustrate characteristic examples of the early days of research in neuroscience. Most scientific figures presented by the neuroanatomists of the time were their own drawings; microphotography was not yet a well-developed technique. Therefore, a successful neuroanatomist required a combination of artistic talent and an ability to interpret microscopic images effectively. The problem was that these illustrations were not necessarily free of technical errors and they may have been subject to the scientists’ own interpretations. Indeed, in some cases, these drawings were considered to be basically artistic interpretations rather than accurate copies of the histological preparations. Furthermore, there are many examples showing that even using the same microscopes and the same techniques, scientists “see” differently through the microscope. As a result, this period of scientific “art” and skepticism represents a fascinating page in the history of neuroscience as it provided the basis of our current understanding of the anatomy of the nervous system.
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Caillaud, Catherine, and Frédéric Sedel. Neuronal Ceroid Lipofuscinoses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0059.
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Neuronal ceroid lipofuscinoses (NCLs) are inherited neurodegenerative disorders beginning mainly in childhood, rarely in adults. They are characterized by the accumulation of autofluorescent lipopigments in brain, especially in neurons. Their clinical heterogeneity is now explained by the huge number of genes (from CLN1 to CLN14) involved in their pathogenesis. Their diagnosis is possible using enzymatic tests and/or direct sequencing of the corresponding genes. Different therapeutic approaches are in development for these diseases such as enzyme replacement therapy or gene transfer.
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Levine, Michael S., Elizabeth A. Wang, Jane Y. Chen, Carlos Cepeda, and Véronique M. André. Altered Neuronal Circuitry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0010.
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In mouse models of Huntington’s disease (HD), synaptic alterations in the cerebral cortex and striatum are present before overt behavioral symptoms and cell death. Similarly, in HD patients, it is now widely accepted that early deficits can occur in the absence of neural atrophy or overt motor symptoms. In addition, hyperkinetic movements seen in early stages are followed by hypokinesis in the late stages, indicating that different processes may be affected. In mouse models, such behavioral alterations parallel complex biphasic changes in glutamate-mediated excitatory, γ-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission and dopamine modulation in medium spiny neurons of the striatum as well as in cortical pyramidal neurons. The progressive electrophysiologic changes in synaptic communication that occur with disease stage in the cortical and basal ganglia circuits of HD mouse models strongly indicate that therapeutic interventions and strategies in human HD must be targeted to different mechanisms in each stage and to specific subclasses of neurons.
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Coleman, William L., and R. Michael Burger. Extracellular Single-Unit Recording and Neuropharmacological Methods. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199939800.003.0003.
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Small biogenic changes in voltage such as action potentials in neurons can be monitored using extracellular single unit recording techniques. This technique allows for investigation of neuronal electrical activity in a manner that is not disruptive to the cell membrane, and individual neurons can be recorded from for extended periods of time. This chapter discusses the basic requirements for an extracellular recording setup, including different types of electrodes, apparatus for controlling electrode position and placement, recording equipment, signal output, data analysis, and the histological confirmation of recording sites usually required for in vivo recordings. A more advanced extracellular recording technique using piggy-back style multibarrel electrodes that allows for localized pharmacological manipulation of neuronal properties is described in detail. Strategies for successful signal isolation, troubleshooting advice such as noise reduction, and suggestions for general laboratory equipment are also discussed.
Book chapters on the topic "Neuronal NOS"
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Masters, B. S. S., K. McMillan, J. Nishimura, P. Martasek, L. J. Roman, E. Sheta, S. S. Gross, and J. Salerno. "Understanding the Structural Aspects of Neuronal Nitric Oxide Synthase (NOS) Using Microdissection by Molecular Cloning Techniques." In Advances in Experimental Medicine and Biology, 163–69. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9480-9_22.
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Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick, et al. "Neuronal Nitric Oxide Synthase (nNOS)." In Encyclopedia of Behavioral Medicine, 1326. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_101144.
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Aoun, Mario Antoine. "STDP within NDS Neurons." In Advances in Neural Networks - ISNN 2010, 33–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13278-0_5.
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Saini, Rashmi, Zaffar Azam, Leena Sapra, and Rupesh K. Srivastava. "Neuronal Nitric Oxide Synthase (nNOS) in Neutrophils: An Insight." In Reviews of Physiology, Biochemistry and Pharmacology, 49–83. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/112_2021_61.
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Grosu, Anca-Ligia, Elmar Oestreicher, Claudius Fauser, Christianto Lumenta, Wolfgang J. Arnold, and Michael Molls. "Vestibular Schwannoma (Acoustic Neuroma)." In Radiotherapy for Non-Malignant Disorders, 629–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-68943-0_36.
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Gattass, Ricardo, Juliana G. M. Soares, and Bruss Lima. "Modulation of Pulvinar Neuronal Activity by Arousal." In The Pulvinar Thalamic Nucleus of Non-Human Primates: Architectonic and Functional Subdivisions, 49–51. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70046-5_10.
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Moon, Cheil, Samhwan Kim, Jisub Bae, and Gabriele V. Ronnett. "Neurobiology and Cultivation of Olfactory Receptor Neurons on a Chip." In Bioelectronic Nose, 97–113. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8613-3_6.
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Schultens, H. A., and D. Schild. "Biophysical Properties of Olfactory Receptor Neurones." In Sensors and Sensory Systems for an Electronic Nose, 13–24. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-015-7985-8_2.
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Ernesto, Burattini. "NES: a Neuron-like net for a diagnostic Expert System." In International Neural Network Conference, 675. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0643-3_41.
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Khedr, Haitham, James Ferlez, and Yasser Shoukry. "PEREGRiNN: Penalized-Relaxation Greedy Neural Network Verifier." In Computer Aided Verification, 287–300. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81685-8_13.
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AbstractNeural Networks (NNs) have increasingly apparent safety implications commensurate with their proliferation in real-world applications: both unanticipated as well as adversarial misclassifications can result in fatal outcomes. As a consequence, techniques of formal verification have been recognized as crucial to the design and deployment of safe NNs. In this paper, we introduce a new approach to formally verify the most commonly considered safety specifications for ReLU NNs – i.e. polytopic specifications on the input and output of the network. Like some other approaches, ours uses a relaxed convex program to mitigate the combinatorial complexity of the problem. However, unique in our approach is the way we use a convex solver not only as a linear feasibility checker, but also as a means of penalizing the amount of relaxation allowed in solutions. In particular, we encode each ReLU by means of the usual linear constraints, and combine this with a convex objective function that penalizes the discrepancy between the output of each neuron and its relaxation. This convex function is further structured to force the largest relaxations to appear closest to the input layer; this provides the further benefit that the most “problematic” neurons are conditioned as early as possible, when conditioning layer by layer. This paradigm can be leveraged to create a verification algorithm that is not only faster in general than competing approaches, but is also able to verify considerably more safety properties; we evaluated PEREGRiNN on a standard MNIST robustness verification suite to substantiate these claims.
Conference papers on the topic "Neuronal NOS"
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Cecílio, Samyra Giarola, Jéssica Naiara Lara, Camila Raianna Justiniana Rocha, and Juliana Pereira Cardoso. "EPILEPSIAS E A HOMEOSTASE DE CLORETO." In II Congresso Brasileiro de Ciências Biológicas On-line. Revista Multidisciplinar Educação e Meio Ambiente, 2021. http://dx.doi.org/10.51189/rema/1662.
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Introdução: Os íons sódio, potássio, cálcio e cloreto são os principais envolvidos na determinação do potencial de membrana das células neuronais. Uma vez que o potencial de equilíbrio do cloreto (ECl), de - 80 mV, é próximo ao potencial de repouso da membrana (- 75 mV), pequenas variações na concentração intracelular do íon interferem de modo significativo no gradiente transmembrânico e, consequentemente, na excitabilidade celular. Objetivo: A proposta do presente estudo consistiu em uma revisão da literatura sobre a influência do desequilíbrio iônico de cloreto. Método: Realizou-se levantamento bibliográfico dos últimos 20 anos (2000- 2020) por meio da busca “chloride” AND “epilepsy” Resultados: A concentração intracelular de cloreto ([Cl-]i) determina a força do sistema de inibição ativado pelos receptores GABAA. Os canais ativados por estes receptores são permeáveis ao íon cloreto. O neurotransmissor GABA possui ação predominantemente inibitória no SNC, porém, as mudanças conformacionais desencadeadas pela ligação do neurotransmissor a estes receptores permitem que haja um influxo ou efluxo de cloreto através dos canais, resposta que será variável conforme a [Cl-]i e o potencial de equilíbrio do íon. Nos neurônios imaturos, nos quais a [Cl-]i é elevada, o ECl é positivo em relação ao Vm, e com a abertura de canais iônicos ativados por GABA, ocorre o efluxo de íons cloreto e despolarização neuronal, com a geração de respostas excitatórias. Esta característica é fundamental para o desenvolvimento neuronal. Inversamente, no cérebro adulto, o cloreto intracelular é mantido a baixas concentrações nos neurônios, sendo a [Cl-]i cerca de 10 a 20 vezes menor do que a concentração extracelular. Nessas condições, ECl é negativo em relação ao Vm e, quando os receptores GABAA são ativados, há o influxo de cloreto e hiperpolarização da membrana neuronal. Durante uma crise epiléptica, a [Cl-]i pode chegar a 26 mM. A falha do sistema de inibição e a despolarização gerada pela alta concentração intracelular acentuam o disparo neuronal, bem como a probabilidade de ocorrência e gravidade das crises. Conclusão: O aumento da [Cl-]i no cérebro aumenta a excitabilidade e os disparos neuronais, favorecendo a ocorrência de crises epilépticas.
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Azevedo, José Bruno da Silva, and JOSÉ BRUNO DA SILVA AZEVEDO. "REVISÃO BIBLIOGRÁFICA SOBRE A DOENÇA DO ALZHEIMER: HIPERFOSFORILAÇÃO DA PROTEÍNA TAU E DEPOSIÇÃO DO PEPTÍDEO β-AMILOSE." In I Congresso Nacional de Pesquisas e Estudos Genéticos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/geneticon/8830.
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Introdução: A doença de Alzheimer é multifatorial ou poligênica e corresponde a cerca de 50 a 75 % de casos de demência nos seres humanos. A proteína TAU é importante na patogenia da demência frontotemporal e para o citoesqueleto neuronal. Essa proteína consegue interagir com a α- e βglobulina para estabilizar os microtúbulos que são essenciais no transporte axonal, na plasticidade sináptica e na manutenção da estrutura neural. Objetivos: Esse trabalho teve como objetivo conhecer as proteínas e os genes promotores no desenvolvimento da doença de alzheimer. Metodologia: Foi realizada uma busca simples nos bancos de dados da SciELO, PubMed e Periódicos Capes, por meio de palavras-chave: “doença de Alzheimer”, “proteína TAU” e “demência frontotemporal”. Foram revisados artigos publicados nos anos de 2009 à 2021. Resultados: A proteína TAU é encontrada montada na doença de alzheimer e os MNFs possuem filamentos emparelhados nos FHA. Os fatores de risco são: a presença do alelo ε4 do gene da apolipoproteína E APOE, do gene da proteína APP no cromossomo 21 e dos genes Presenilinas 1 e 2 nos cromossomos 14 e 1. A TAU faz sua própria polimerização e inibe a despolimerização rápida da tubulina, esse processo é regulado pelo estado de fosforilação da proteína TAU, que compreende aproximadamente 79 sítios de fosforilação em resíduos de serina e treonina. O equilíbrio entre fosforilação e desfosforilação dos epítopos promove alterações que influenciam como a proteína TAU interage com a α- e β-tubulina que estabilizam os microtúbulos nos neurônios. Várias proteínas quinases e fosfatases estão envolvidas na regulação da fosforilação da TAU, sendo a enzima glicogênio sintase quinase 3β GSK3β a mais importante TAU quinase nos neurônios. A redução da expressão de certas fosfatases também é identificada nos tecidos cerebrais de pacientes com alzheimer. Conclusão: A TAU hiperfosforilada intraneural pode ser encontrada no cérebro de indivíduos com demência muito leve, não acompanhada de patologia β-amiloide. A hiperfosforilação de TAU pode ser um evento precoce na fisiopatologia do alzheimer, enquanto outros mecanismos patológicos, incluindo superprodução da Aβ e ativação de cascatas inflamatórias e estresse oxidativo, podem ser secundários à disfunção geral na homeostase neuronal.
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Junkes, Giovanna Braz, Diego Akyo Hoshina dos Santos, Julia Petry, and Meria Eduarda Mendes Hibarino. "A ATROFIA NEURONAL E SUA RELAÇÃO COM A DOENÇA DE ALZHEIMER." In I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/81.
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Introdução: O Alzheimer é uma patologia neurodegenerativa que afeta o Sistema Nervoso Central por causar atrofia neuronal derivada do acúmulo do peptídeo Beta Amilóide e da proteína Tau. A doença é comumente associada à idade e caracteriza-se pela demência, apresentando sintomas como disfunções na cognição e distúrbios comportamentais e na memória. Objetivo: O objetivo desse trabalho é informar sobre aspectos fisiopatológicos da doença de Alzheimer e esclarecer minimamente como ocorre o seu desenvolvimento. Material e métodos: Trata-se de uma revisão bibliográfica baseada em artigos, escritos em inglês e português, encontrados no PubMed e na Revista Episteme Transversalis no período entre 2020 e 2021. Resultados: Com base nos artigos encontrados, foi possível observar que no mal de Alzheimer evidencia-se agregados do peptídeo Beta Amilóide e uma hiperfosforilação da proteína Tau. O Beta Amilóide é formado a partir da clivagem da proteína precursora amilóide (PPA), processo que pode ocorrer de duas formas, sendo que a via normal, não amiloidogênica, não gera Beta Amilóide. Porém, na via amiloidogênica, a PPA é clivada pela enzima beta-secretase e, posteriormente, pela gama-secretase, tendo como produto um peptídeo com 40 ou 42 aminoácidos que é insolúvel e tende a agregar-se. Esse peptídeo com 42 aminoácidos é tóxico, pois ao se agrupar pode causar alterações na função cognitiva. Ocorre então, em resposta ao grande acúmulo de peptídeos, uma hiperativação de quinases e hipoativação de fosforilases que resultam em um aumento significativo na fosforilação da proteína Tau, o que provoca mobilização da micróglia e liberação de citocinas inflamatórias, causando atrofia neuronal e morte celular. O desenvolvimento de toxicidade impede o transporte axonal, colaborando com o progresso dos déficits cognitivos que evidenciam demência. Conclusão: A partir dessa revisão bibliográfica pode-se concluir que a atrofia neuronal, resultante do acúmulo do peptídeo Beta Amilóide e fosforilação exarcebada da proteína Tau, é uma patologia correlacionada com a doença de Alzheimer e com os déficits cognitivos observados no decorrer da enfermidade.
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Costa, Luisy Karen Lemos, Caio Marques Da Silva, Bárbara Monique De Freitas Vasconcelo, Fernanda Fonsêca Monteiro Freire, and Juliana Minervina De Souza Freire. "ALZHEIMER E SUAS BASES FISIOPATOLÓGICAS." In II Congresso Brasileiro de Saúde On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1505.
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Introdução: A doença do Alzheimer (DA) é uma doença neurodegenerativa crônica, na qual causa deterioração cognitiva de forma progressiva. O processo fisiopatológico e os sintomas são ocasionados em virtude da morte das células nervosas e perda de tecido em todo o cérebro, isso se dá devido ao mal funcionamento das proteínas Beta-amiloide e Tau. Objetivos: Compreender a fisiopatologia associada a doença de Alzheimer. Material e métodos: Foi realizada uma revisão de literatura integrativa usando os bancos de dados Revista Brasileira de Neurologia e Scielo, aplicando os descritores “Doença de Alzheimer”; “Fisiopatologia Alzheimer” e “Sinais e sintomas do Alzheimer”. Usou-se como critério de inclusão os artigos em inglês e português que estivessem no período entre os anos de 2015 a 2021. Resultados: O acúmulo das proteínas Beta-amiloide e Tau, forma placas e emaranhados em regiões específicas do cérebro que inibem as sinapses neuronais necessárias para o funcionamento do sistema nervoso central. A localização dessas proteínas, determinam os sinais e sintomas da Doença de Alzheimer, ocasionando lesões permanentes a nível celular, como a degeneração neurofibrilar que condiz ao espessamento e tortuosidade nas células neurofibrilas localizadas no pericário neuronal, podendo alterar os constituintes celulares gerais. As proteínas beta-amiloide estão relacionadas no auxílio do sistema imunológico nervoso central, que atuam na captura de microrganismos que passagem pela barreira hematoencefálica, a forma deficiente desta proteína ocasiona inúmeras alterações nas células nervosas, principalmente a destruição dos dendritos que são as projeções comunicantes nos neurônios. Em células nervosas saudáveis, a proteína tau contribui na formação e estabilização dos microtúbulos, os quais são fundamentais para a comunicação entre os neurônios. Nos pacientes com a doença de Alzheimer a proteína tau para de funcionar corretamente, pois separa-se dos microtúbulos e criam formas desorganizadas que irão obstruir os microtúbulos. Conclusão: Diante das inibições de sinapses neuronais, as células cerebrais se degeneram e morrem, gerando perda de memória e algumas funções mentais. Além de ser uma doença degenerativa tão invasiva, é necessário promover uma melhor qualidade de vida para os pacientes, um esforço conjunto entre a família e os profissionais da saúde, como fisioterapeuta, fonoaudiólogo, psicólogo, nutricionista, terapeuta ocupacional, entre outros.
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Paz, Cândida Verônica de Andrade, EDUARDA MARTINS DOS SANTOS, TÁSSIA AIMÊ TEIXEIRA NASCIMENTO, RAFAEL PEREIRA CAMARGO, and LAURI PAULO MALACARNE JUNIOR. "CONFORMAÇÕES GENÉTICAS E IMUNOLÓGICAS DA DOENÇA DE ALZHEIMER." In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6783.
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Introdução: A doença de Alzheimer (DA) é uma patologia neurodegenerativa irreversível e a principal causa de demência na senescência. Essa doença é caracterizada por lesões cerebrais responsáveis pelo controle da memória e funções cognitivas. Estudos apontam uma relação aparente em alterações gênicas, fatores ambientais, bem como nos processos imunológicos interconectados a principais interleucinas. Objetivo: Analisar aspectos imunogenéticos envolvidos na DA. Material e métodos: Revisão narrativa de literatura nas plataformas científicas PUBMED, SCIELO e MEDLINE. Como critério de busca para seleção dos estudos elegíveis foram aplicadas os unitermos: “alzheimer” AND “mutação” AND “imunologia” AND “genética”. Foram identificados 153 artigos publicados entre 2016 a 2022, nos idiomas português e inglês e após a leitura avaliativa dos resumos dos estudos, 11 trabalhos científicos foram elencados para a produção do presente trabalho. Foram desconsiderados estudos repetidos ou que não atendiam a temática. Resultados: Verificou-se que a DA é destacada pela complexidade de fatores genéticos associados, sendo a neurodegeneração relacionada a alterações no processo de splicing alternativo, onde íntrons passam a executar função codificadora no mRNA. Estudos em animais apontam que mutações nos genes que codificam a DNA polimerase, proteína chave no reparo do DNA, podem acarretar em doenças com o fenótipo de envelhecimento acelerado, resultando em uma disfunção e perda neuronal por meio da privação de energia, a qual é oriunda tanto do descarrilamento metabólico quanto do acúmulo de mitocôndrias danificadas. Biomarcadores inflamatórios, como a interleucina-10 (IL-10), mostram-se com níveis séricos baixos relacionados com a DA. Observaram-se, também, alterações significativas ao nível das células B, as quais nos doentes apresentavam uma expressão aumentada dos marcadores CD69 e CD40, moléculas co-estimuladoras essenciais para troca de classe de imunoglobulina. Conclusão: Sendo assim, fica evidente o papel dos fatores de riscos genéticos e relacionados à imunidade que se convergem para o surgimento e agravamento da neurodegeneração, bem como da neuroinflamação, processos estes que podem ser desacelerados com tratamentos, terapias e mudanças no estilo de vida. Todavia, mais estudos moleculares são necessários para o manejo da solução e prevenção desta patologia.
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García de Mateos Sanchis, Claudia. "Retrato de una Cerilla. El Ensayo Audiovisual como Posicionamiento Crítico en la Sociedad del Rendimiento." In II Congreso Internacional Estéticas Híbridas de la Imagen en Movimiento: Identidad y Patrimonio. Valencia: Universitat Politàcnica de València, 2021. http://dx.doi.org/10.4995/eshid2021.2021.13219.
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Byung-Chul Han, en La sociedad de la transparencia (2013), describe el síndrome psíquico de Burnout. En resumen, es un estado de agotamiento físico, emocional o mental, un cansancio emocional que provoca la despersonalización, con consecuencias para la autoestima así como la pérdida del interés y el sentido de la responsabilidad. Esta situación ha sido provocada y aprovechada por el neocapitalismo liberal, ofreciendo la oportunidad de suplir ese vacío existencial con la realización personal a través del trabajo, de la producción. Sin embargo, para hacer esto posible, no se ejerce una violencia física externa que obliga, propia de una sociedad disciplinaria, sino que viene de una voz interna identificada como personal y propia que repite en bucle que siempre es posible hacer un poco más para llegar un poco más alto y ser un poco mejor que ayer. ¿Cuál es el origen de esta necesidad? ¿Es natural la constante propuesta de superación y mejora? ¿Es posible detectar y parar esos mecanismos neuronales que obligan al sujeto a rendir hasta límites insanos física y mentalmente? Retrato de una cerilla. Bloque I: Identificación es un ensayo audiovisual que conforma la primera parte de una investigación audiovisual compuesta de cuatro bloques transdisciplinares en relación con los mecanismos individuales y sociales que potencian la violencia neuronal derivada del autorrendimiento. El proyecto nos plantea una cuestión clara: ¿la autoexigencia que se ha llegado a comprender como parte intrínseca de la personalidad es natural o es, por el contrario, un comportamiento inducido y naturalizado hasta el punto de hacerlo pasar como propio? A través de las aportaciones conceptuales y formales de lenguajes audiovisuales tales como el apropiacionismo y el uso de montajes de corte rítmico e intelectual, Retrato de una cerilla defiende el arte como crítica y resistencia al nuevo modelo de sociedad derivado del neocapitalismo postmoderno.
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Nogueira, Raniery Augusto dos Santos Beserra, Ana Beatriz Silva Barbosa, Francisco Das Chagas Diassis Jácome Valentim, Sâmya Pires Batista De Azevêdo, and Jamile Rodrigues Cosme De Holanda. "MECANISMOS DE MANUTENÇÃO DA LATÊNCIA DO VÍRUS VARICELA ZÓSTER: UMA ADAPTAÇÃO NECESSÁRIA." In I Congresso Nacional de Microbiologia Clínica On-Line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1182.
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Introdução: O Vírus Varicela Zóster pertence à subfamília α-herpesviridae e é um DNA-vírus de fita dupla, possuindo 68 Fases de Leitura Aberta (ORF) únicas. Sendo responsável por varicela, em um primeiro contato, o vírus mantém-se latente por um longo período em gânglios das raízes dorsais e de nervos cranianos, disseminando-se por essas estruturas após décadas, quando reativado, configurando Herpes Zóster, cujas complicações prejudicam a qualidade de vida dos pacientes. Posteriormente à infecção primária, o vírus classifica-se como neurotrópico e seus meios de sobrevida em neurônios, ainda não são claros. Objetivo: Este estudo busca elucidar os mecanismos de latência desse patógeno, visando ao desenvolvimento do conhecimento científico no assunto. Material e Métodos: Utilizando-se da plataforma online PubMed, foram pesquisados os descritores “varicella zoster virus”, em adição a “apoptosis”, e “herpes zoster infection”, com o operador booleano “AND” tendo como filtro a delimitação temporal entre 01/01/2018 e 01/05/2021. Resultados: Ao longo do período de latência, o DNA viral é encontrado em células neuronais, estando em forma não-integrada (cita-se epissoma infinito ou comprimento concateméro) e sua transcrição é fortemente restrita. Em meio ao genoma viral, o ORF63 mostrou-se de grande relevância na proteção de neuronal em humanos. Durante monitorização, foi-se percebido a migração da proteína OFR63 quando se induz apoptose na célula, tornando-se mais citoplasmática. A partir disso, percebeu-se interação inibitória entre a proteína ORF63 e a estaurosporina, molécula indutora da apoptose. O que até então se mostrava como hipótese, foi melhor embasado pela redução dos níveis de caspase-3, marcador apoptótico celular, em neurônios infectados pelo VVZ quando comparados a outras células (infectadas ou não). Conclusão: Diante de todas as questões, ainda cientificamente obscuras, acerca da capacidade desse vírus de sobreviver durante décadas nos gânglios nervosos, ressalta-se a necessidade de mais pesquisas na área, para que se tenha melhor manejo de pacientes infectados com o Vírus Varicela Zóster. Ademais, não se pode negar que a inibição da apoptose é uma evolução adaptativa muito favorável ao microrganismo, já que as células neuronais são hospedeiras senescentes e seu aumento de vida significa aumento de vida do patógeno.
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Silva, Arthur Gonsales, Gabriel Freitas Damasceno, Adrielle do Espírito Santo Macedo, Fernando Allan de Farias Rocha, and Bruno Duarte Gomes. "Detecção de Artefatos em Eletroencefalografia usando Árvores de Decisão com Gradiente Impulsionado." In Congresso Brasileiro de Inteligência Computacional. SBIC, 2021. http://dx.doi.org/10.21528/cbic2021-153.
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Em estudos de processamento digital de sinais e aprendizado de máquina aplicados a registros de Eletroencefalografia (EEG) de pacientes portadores de epilepsia, pesquisadores normalmente necessitam de um método automatizado e acurado para detectar e/ou discriminar padrões artefatuais em seguimentos de dados, uma vez que métodos manuais e baseados em conhecimento de domínio são altamente passíveis de erro e viés. Muitos métodos vem sendo empregados em tarefas de detecção e classificação de sinais de EEG, porém a grande maioria destas estratégias, quando consideradas de alta eficiência, requerem considerável poder de armazenamento e processamento computacionais, uma vez que dados de atividade neuronal possuem grande complexidade associada. Como uma alternativa à abordagens mais complexas, neste trabalho visamos desenvolver um método de mais baixo custo computacional para discriminação de padrões artefatuais em registros de EEG de pacientes com epilepsia, utilizando a Transformada de Hilbert-Huang (HHT) e um conjunto de estatísticas paramétricas e não paramétricas para extração de informação das amostras, juntamente com um modelo ensemble, baseado em Árvores de Decisão (AD) para discriminação entre três tipos diferentes de padrões artefatuais nos seguimentos de dados.
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Vasconcelos, beatriz Lopes de, RICHARD TARCÍSIO DE LIMA ALVES, and WANDERLEYA MEDEIROS. "TRATAMENTO NEONATAL DE CRIANÇAS DIAGNOSTICADAS COM HIPOTIREOIDISMO CONGÊNITO." In III Congresso Brasileiro de Ciências Biologicas. Revista Multidisciplinar de Educação e Meio Ambiente, 2022. http://dx.doi.org/10.51189/iii-conbracib/6370.
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INTRODUÇÃO: O hipotireoidismo congênito é uma das razões mais comuns para o retardo mental e desenvolvimento corporal de crianças. Pode-se impedir o desenvolvimento neurológico destas em seus primeiros anos de vida, devido uma má formação na glândula tireoide durante a gestação. Mediante tal situação, é imprescindível o diagnóstico precoce e o tratamento neonatal. OBJETIVO: Avaliar o desenvolvimento de crianças com hipotireoidismo congênito em tratamento neonatal desde seus primeiros dias de existência. METODOLOGIA: Trata-se de um estudo de revisão narrativa, realizada a partir de pesquisas conduzidas em pacientes diagnosticados com tal doença, sendo tratados desde o nascimento. RESULTADOS: Hipotireoidismo congênito é uma das causas mais comuns de retardo mental passível de prevenção, o tratamento farmacológico é feito pela reposição do hormônio tireoidiano, tetraiodotironina - T4, um dos principais hormônios responsáveis pelo desenvolvimento do ser humano. É através do Teste do pézinho, realizado nos primeiros dias de vida do bebê, de 48 horas ao 5° dia, que se obtém o diagnóstico, além de outras doenças como fenilcetonúria, síndromes falciformes, fibrose cística, hiperplasia adrenal congênita e deficiência de biotinidase. A causa mais comum para o hipotireoidismo congênito é um defeito na formação e desenvolvimento da tireoide do bebê, ainda dentro do útero da mãe. O tratamento com levotiroxina (LT4) deve ser iniciado nos primeiros dias, com o objetivo de manter os níveis de tireotropina (TSH) e hormônio tireoidiano livre na faixa normal. Altas doses de levotiroxina foram usadas para um melhor resultado do tratamento neonatal. A dosagem inicial elevada de LT4 foi eficaz e atingiu com segurança o desenvolvimento cognitivo ideal em crianças com hipotireoidismo congênito, incluindo aqueles gravemente afetados. CONCLUSÃO: As crianças seguindo o tratamento de reposição hormonal de levotiroxina não tiveram grandes diferenças de peso, altura e maturação óssea se comparadas às outras crianças que não possuem deficiência na tireoide. Nos primeiros anos, o desenvolvimento neuronal aconteceu normalmente com a dosagem alta de LT4, resultando numa melhora significativa no quociente de inteligência.
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Marques, Daiane Silva, Roseane Oliveira Veras, Maria Dhescyca Ingrid Silva Arruda, João Felipe Tinto Silva, and Francisco Lucas de Lima Fontes. "REPERCUSSÕES CLÍNICAS E FISIOPATOLÓGICAS DA DOENÇA DE HUNTINGTON: REVISÃO INTEGRATIVA DA LITERATURA." In II CONGRESSO ON-LINE NACIONAL DE CIÊNCIAS & SAÚDE (II CONCS). Literacia Cientifica Editora & Cursos, 2022. http://dx.doi.org/10.53524/lit.edt.978-65-84528-09-3/72.
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INTRODUÇÃO: A Doença de Huntington (DH) é considerada uma patologia neurodegenerativa, crônica, letal, com herança autossômica dominante que codifica a proteína huntingtina e caracteriza-se por diversas repercussões clínicas como: coreia progressiva, diminuição da cognição, depressão, dentre outras. Habitualmente, a DH manifesta-se entre 30 a 50 anos, no entanto, tem possibilidade de ocorrer o fenômeno de antecipação (Huntington juvenil), atingindo jovens e crianças. Ainda não possui cura para a DH, contudo, apresenta tratamento. OBJETIVO: Apresentar os aspectos clínicos e fisiopatológicos da DH. MÉTODOS: Trata-se de uma abordagem qualitativa de revisão integrativa da literatura, efetuada em fevereiro de 2022, em que a pergunta norteadora foi fundamentada no acrônimo PICo (População, Interesse e Contexto), definida como: Quais são as repercussões clínicas e fisiopatológicas da DH? A pesquisa foi executada nas bases de dados: Literatura Latino-americana e do Caribe em Ciências da Saúde (LILACS), Medical Literature Analysis and Retrieval System Online (MEDLINE) via Biblioteca Virtual em Saúde (BVS) e Science Direct. Utilizaram-se os seguintes Descritores em Ciências da Saúde (DeCS) e Medical Subject Headings (MeSH): “Doença de Huntington”, “Huntington Disease” “Proteína Huntingtina”, “Huntingtin Protein”, “Glutamina” e “Glutamine”. As estratégias de busca foram formuladas baseadas nos descritores mencionados, aplicando o operador booleano “AND”. Os critérios de inclusão compreenderam: estudos disponíveis na íntegra, estudos observacionais, revisões sistemáticas e capítulos de livros no idioma português e inglês, no período de 2013 a 2018, com a finalidade de encontrar evidências atuais acerca da temática. Excluíram-se, monografias, teses, artigos incompletos, indisponíveis e aqueles que não tinham correlação ao objetivo. Desse modo, foram identificados 891 estudos, dos quais, após a utilização dos critérios de elegibilidade e exclusão, restaram 235 estudos. Posteriormente a realização da leitura dos títulos e resumos, somente 10 responderam a finalidade da revisão. RESULTADOS: Diante das evidências científicas analisadas, clinicamente, a DH caracteriza-se por coreia progressiva (movimentos involuntários), declínio cognitivo e implicações psiquiátricas. Nos estágios iniciais, observa-se irritabilidade, depressão e alterações motoras, estas associadas à perda de coordenação dos movimentos voluntários. Já os movimentos involuntários tornam-se mais severos, implicando na piora da mobilidade e cognição. Em indivíduos jovens, a repercussão clínica é distinta, sendo representada por bradicinesia, tremores, rigidez e distonia. Durante a evolução da DH, a disfunção intracelular provocada pela huntingtina mutante implica na degeneração de relevantes vias neuronais e aniquilamento celular no corpo estriado, córtex cerebral e demais áreas do cérebro. A DH não é baseada, necessariamente, no impacto direto da proteína mutante, possui também mecanismos de excitotoxicidade, toxicidade dopaminérgica, desregulação do metabolismo, disfunção mitocondrial, estresse oxidativo, apoptose e autofagia, fatores estes que compõem a fisiopatologia da DH. Alguns destes mecanismos, além do desenvolvimento gradativo, acentuamse tardiamente na doença, podendo até levar à morte neuronal. CONCLUSÃO: Percebe-se que a DH possui evolução crônica e progressiva. Até o momento, não apresenta possibilidade de cura, entretanto, existe tratamento multiprofissional. Assim, além da avaliação, é necessário compreender os aspectos clínicos e fisiopatológicos, para que o tratamento proporcione uma qualidade de vida eficaz nestes pacientes.
Reports on the topic "Neuronal NOS"
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Quintero Ramírez, Nini, Yuris Sánchez García, Yasmina Toncel, and Liliana Reales Hernández. Estimulación táctil kinestésica: abordaje desde enfermería. Ediciones Universidad Cooperativa de Colombia, August 2021. http://dx.doi.org/10.16925/gcnc.17.
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La supervivencia de neonatos que no cumplen su desarrollo gestacional completo (< 34 semanas) se ve sometida a técnicas que estimulan su desarrollo neuronal. Por lo tanto, se da a conocer la técnica de estimulación táctil kinestésica, que consiste en desarrollar los estímulos sensoriales del neonato; así mismo, se describe cómo llevar a cabo ese proceso y el aprendizaje adquirido por los neonatos. El presente documento hace un abordaje grosso modo de la técnica de estimulación táctil kinestésica de acuerdo con algunos autores que han investigado acerca de la temática.
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Morphett, Jane, Alexandra Whittaker, Amy Reichelt, and Mark Hutchinson. Perineuronal net structure as a non-cellular mechanism of affective state, a scoping review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0075.
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Is the perineuronal net structure within emotional processing brain regions associated with changes in affective state? The objective of this scoping review is to bring together the literature on human and animal studies which have measured perineuronal net structure in brain regions associated with emotional processing (such as but not limited to amygdala, hippocampus and prefrontal cortex). Perineuronal nets are a specialised form of condensed extracellular matrix that enwrap and protect neurons (Suttkus et al., 2016), regulate synaptic plasticity (Celio and Blumcke, 1994) and ion homeostasis (Morawski et al., 2015). Perineuronal nets are dynamic structures that are influenced by external and internal environmental shifts – for example, increasing in intensity and number in response to stressors (Blanco and Conant, 2021) and pharmacological agents (Riga et al., 2017). This review’s objective is to generate a compilation of existing knowledge regarding the structural changes of perineuronal nets in experimental studies that manipulate affective state, including those that alter environmental stressors. The outcomes will inform future research directions by elucidating non-cellular central nervous system mechanisms that underpin positive and negative emotional states. These methods may also be targets for manipulation to manage conditions of depression or promote wellbeing. Population: human and animal Condition: affective state as determined through validated behavioural assessment methods or established biomarkers. This includes both positive and negative affective states. Context: PNN structure, measuringPNNs.
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Andrades, Oscar, David Ulloa, Dario Martinez, Francisco Guede, Gustava Muñoz, Luis Javier Chirosa, and Amador García. Effect of the manipulation of the variables that configure the stimulus of strength training on motor symptoms in people with Parkinson's disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0079.
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Review question / Objective: To analyze the evidence on studies that have manipulated the variables that make up the strength training stimulus and its effects on motor symptoms in people with Parkinson's disease. Condition being studied: Parkinson's is a multisystemic neurodegenerative disease that affects the central nervous system and is caused by a loss of dopaminergic neurons in the compact part of the substantia nigra of the basal ganglia of the midbrain. People with Parkinson's disease (PEP) have non-motor and motor clinical symptoms. Classic motor symptoms are rest tremor, joint stiffness, bradykinesia, decreased balance, gait disturbances (speed, temporality, spatiality, support, and freezing) and decreased functional performance.
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Gothilf, Yoav, Roger Cone, Berta Levavi-Sivan, and Sheenan Harpaz. Genetic manipulations of MC4R for increased growth and feed efficiency in fish. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7600043.bard.
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The hypothalamic melanocortin system plays a central role in the regulation of food consumption and energy homeostasis in mammals. Accordingly, our working hypothesis in this project was that genetic editing of the mc4r gene, encoding Melanocortin Receptor 4 (MC4R), will enhance food consumption, feed efficiency and growth in fish. To test this hypothesis and to assess the utility of mc4r editing for the enhancement of feed efficiency and growth in fish, the following objectives were set: Test the effect of the mc4r-null allele on feeding behavior, growth, metabolism and survival in zebrafish. Generate mc4r-null alleles in tilapia and examine the consequences for growth and survival, feed efficiency and body composition. Generate and examine the effect of naturally-occurring mc4r alleles found in swordfish on feeding behavior, growth and survival in zebrafish. Define the MC4R-mediated and MC4R-independent effects of AgRP by crossing mc4r- null strains with fish lacking AgRP neurons or the agrpgene. Our results in zebrafish did not support our hypothesis. While knockout of the agrpgene or genetic ablation of hypothalamic AgRP neurons led to reduced food intake in zebrafish larvae, knockout (KO) of the mc4r gene not only did not increase the rate of food intake but even reduced it. Since Melanocortin Receptor 3 (MC3R) has also been proposed to be involved in hypothalamic control of food intake, we also tested the effectofmc3r gene KO. Again, contrary to our hypothesis, the rate of food intake decreased. The next step was to generate a double mutant lucking both functional MC3R and MC4R. Again, the double KO exhibited reduced food intake. Thus, the only manipulation within the melanocortin system that affected food intake in consistent with the expected role of the system was seen in zebrafish larvae upon agrpKO. Interestingly, despite the apparent reduced food intake in the larval stage, these fish grow to be of the same size as wildtype fish at the adult stage. Altogether, it seems that there is a compensatory mechanism that overrides the effect of genetic manipulations of the melanocortin system in zebrafish. Under Aim 3, we introduced the Xna1, XnB1l, and XnB2A mutations from the Xiphophorus MC4R alleles into the zebrafish MC4R gene. We hypothesized that these MC4R mutations would act as dominant negative alleles to increase growth by suppressing endogenous MC4R activity. When we examined the activity of the three mutant alleles, we were unable to document any inhibition of a co-transfected wild type MC4R allele, hence we did not introduce these alleles into zebrafish. Since teleost fish possess two agrpgenes we also tested the effect of KO of the agrp2 gene and ablation of the AgRP2 cells. We found that the AgRP2 system does not affect food consumption but may rather be involved in modulating the stress response. To try to apply genetic editing in farmed fish species we turned to tilapia. Injection of exogenous AgRP in adult tilapia induced significant changes in the expression of pituitary hormones. Genetic editing in tilapia is far more complicated than in zebrafish. Nevertheless, we managed to generate one mutant fish carrying a mutation in mc4r. That individual died before reaching sexual maturity. Thus, our attempt to generate an mc4r-mutant tilapia line was almost successful and indicate out non-obvious capability to generate mutant tilapia.
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Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.
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Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.
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Biehl, María Loreto, Raquel Fernández-Coto, and Hazel Elizondo Barboza. Menos violencia, más aprendizaje: Un análisis neurocientífico de jóvenes en Honduras. Inter-American Development Bank, February 2021. http://dx.doi.org/10.18235/0003229.
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La violencia en Latinoamérica forma parte de la cotidianeidad de muchos jóvenes en edad de asistir a la secundaria. Además del efecto que esto acarrea en su rendimiento y asistencia escolar, resulta de interés conocer los efectos a nivel cerebral y las implicaciones que esto puede generar en sus funciones cognitivas. Honduras se perfila como uno de los países con los mayores índices de violencia y criminalidad no solamente a nivel Latinoamericano sino también a nivel mundial. Enmarcado en el contexto anterior, el presente documento presenta los principales hallazgos del estudio neurocientífico El Cerebro Adolescente Expuesto a la Violencia Escolar (2019), realizado por la Universidad Nacional Autónoma de Honduras, específicamente por el Grupo de Investigación de Neurociencias Aplicadas de la Universidad, en colaboración con el Banco Interamericano de Desarrollo. Dicho estudio incluyó 117 estudiantes de edades entre 14 y 17 años de tres centros educativos de secundaria. Los resultados arrojan que efectivamente aquellos estudiantes con exposición más alta a la violencia producen en promedio más cortisol, conocida como la hormona del estrés, que aquellos expuestos a un nivel de violencia bajo. Aunado a lo anterior, se generó evidencia de que la alta exposición a la violencia genera hiperconectividad en las redes neuronales del cerebro, lo que repercute en el desempeño de funciones cognitivas relevantes como son la memoria, la percepción y la atención. Por último, en el área de aprendizaje, los estudiantes con mayor exposición a la violencia obtuvieron resultados más bajos en pruebas estandarizadas de español y matemática, al compararse con aquellos estudiantes con niveles más bajos de exposición a la violencia.