Littérature scientifique sur le sujet « Basi nervose »
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Articles de revues sur le sujet "Basi nervose"
1
Rosa, M. L., M. A. Canevari, N. Mavilio, S. Ballerini, D. Capello, A. Dorcaratto et E. Marinaro. « Tumori cerebrali primitivi ». Rivista di Neuroradiologia 6, no 4 (novembre 1993) : 455–88. http://dx.doi.org/10.1177/197140099300600411.
Texte intégralRésumé :
Nello studio delle neoplasie cerebrali primitive, anche ai fini di una indicazione per quanto riguarda la benignità o malignità delle lesioni, un adeguato inquadramento può essere ottenuto sulla scorta di conoscenze generali che si riferiscono — oltre ovviamente ai dati anamnestici — alla classificazione, al comportamento biologico-grado di malignità, alla localizzazione, ai segni di effetto massa e alla valutazione di elementi più specifici che hanno diretta espressività sulle immagini di TC e di RM quali: gli aspetti istologici, biologici e clinici. Per quanto riguarda gli aspetti istologici bisogna far riferimento alle basi patologiche delle immagini; per gli aspetti biologici alle indicazioni fornite dalle neuroimmagini che si riferiscono al tipo di accrescimento della neoplasia, all'eventuale presenza di metastasi per via liquorale e, più raramente, per via ematogena ed alla comparsa di una recidiva o meglio di una progressione della malattia. Infine è opportuno tenere in debita considerazione l'espressività clinica che comprende, oltre agli aspetti istologici e biologici, anche l'effetto compressivo sulle strutture nervose vitali (effetto massa ed ernie) e sulle vie liquorali ( idrocefalo ostruttivo) che costituiscono un elemento prognostico sfavorevole anche in caso di tumori benigni. Riteniamo quindi che l'espressività-biologica, clinica ed istopatologica in neuroradiologia rappresenti la strada da seguire per un ulteriore miglioramento nella diagnostica dei tumori cerebrali. Nel contempo è necessario ricercare una più approfondita valutazione degli aspetti funzionali mediante RM e PET ai fini di un più completo inquadramento delle lesioni anche sotto questo aspetto.
2
Guirro, Rinaldo R. J. « O uso do ultrassom terapêutico na regeneração de nervos periféricos após lesão por esmagamento ». Fisioterapia Brasil 11, no 5 (9 décembre 2017) : 381. http://dx.doi.org/10.33233/fb.v11i5.1426.
Texte intégralRésumé :
O ultrassom terapêutico (UST) é um recurso não invasivo que pode auxiliar na regeneração nervosa periférica. Objetivo: Revisar os efeitos da aplicação do UST na regeneração de nervos periféricos. Material e métodos: A revisão de literatura não sistemática teve como base de dados Lilacs, Medline, Cochrane e Pubmed, além das consultas em referências de livros e periódicos do acervo da biblioteca da Faculdade de Medicina de Ribeirão Preto. Foram analisadas 66 publicações entre artigos e teses, sendo selecionados 28 trabalhos publicados entre 1994 a 2009. Incluíram-se estudos constando as seguintes dimensões: características da regeneração nervosa, lesões nervosas periféricas por esmagamento, características e aplicação do UST no tratamento de lesões nervosas periféricas. Primeiramente, serão descritas as lesões nervosas periféricas e suas etapas de regeneração, seguido por um breve comentário sobre lesões por esmagamento. A seguir será abordada a aplicação do UST como forma de tratamento em lesões nervosas periféricas. Resultados: A literatura disponível demonstra que o uso do UST no modo pulsado com baixa intensidade foi efi caz no tratamento, acelerando o processo de regeneração. Conclusão: O uso do UST apresentou respostas satisfatórias no processo de regeneração do nervo periférico, sendo necessários maiores estudos para padronizar os parâmetros físicos do UST, da pressão exercida durante a lesão por esmagamento, do período de tratamento e acompanhamento, bem como das análises realizadas. Palavras-chave: regeneração nervosa periférica, lesão por esmagamento, compressão neuropática, ultrassom terapêutico.
3
Castro, Tiane Ferreira de, Daniel Alexandre Stüpp de Souza, Rodolfo Pinho da Silva Filho et Malcon Andrei Martinez Pereira. « Sistematização e distribuição da inervação lombar e sacral em Arctocephalus australis ». Brazilian Journal of Veterinary Research and Animal Science 46, no 5 (1 octobre 2009) : 404. http://dx.doi.org/10.11606/issn.1678-4456.bjvras.2009.26791.
Texte intégralRésumé :
Objetivando descrever a inervação originada a partir dos ramos ventrais lombares e sacrais, fez-se um estudo, mediante a dissecação de dois exemplares de lobos-marinhos (Arctocephalus australis), oriundos do CRAM-FURG, onde chegaram em óbito. As estruturas nervosas constituintes dos plexos lombar e sacral possuem origem dos ramos ventrais dos nervos espinhais que formam-se dos segmentos medulares L1 a S3. Assim, pode-se observar que, os formados dos segmentos L1 a L3 são unissegmentares, sendo respectivamente os nervos Ílio-hipogástrico e Ílio-inguinal e Cutâneo Femoral Lateral. Da união dos segmentos L3-L4 surgem os nervos Genito-femoral, Obturatório e Femoral. Da confluência dos segmentos L4-5-S1 forma-se um tronco nervoso, o plexo isquiático, que emite os nervos: Glúteos Cranial e Caudal, Cutâneo Femoral Caudal e Isquiático. O nervo Isquiático ramifica-se em Cutâneos Surais Lateral e Caudal, Tibial, Fibular Comum. O nervo Pudendo (divide-se nos nervos dorsal do pênis ou clitóris e perineais superficial e profundo) e Retal Caudal têm origem dos segmentos S2-3. Com base nestes dados podemos inferir que a inervação lombar e sacral têm origem similar a outras espécies de mamíferos, contudo sua organização e distribuição refletem as modificações adaptativas aos hábitos destes animais, principalmente a locomoção em meio aquático.
4
Jardim, Edymar, et Osvaldo M. Takayanagui. « Forma nervosa crônica da doença de Chagas : estudo clínico evolutivo e anatomopatológico de um caso seguido durante vinte anos ». Arquivos de Neuro-Psiquiatria 51, no 4 (novembre 1993) : 537–40. http://dx.doi.org/10.1590/s0004-282x1993000400020.
Texte intégralRésumé :
As formas nervosas crônicas da doença de Chagas comprometem tanto o sistema nervoso central (SNC) como o periférico, apesar de não serem encontradas com a frequência assinalada por Chagas em suas observações iniciais. O atual relato refere-se a uma paciente chagásica crônica desde a infância que, progressivamente, desenvolveu comprometimento da motricidade voluntária, do tono muscular, da coordenação, dos nervos cranianos. Sofria ainda de uma cardiopatia e de uma colopatia chagásicas, vindo a falecer no pós-operatório de uma hemicolectomia. Foi necropsiada e o estudo histopatológico do SNC revelou desmielinização dos feixes espinocerebelares e dos cordões posteriores, grande redução do número de células de Purkinje, grande destruição neuronal da substância negra e do locus coeruleus, estado lacunar dos núcleos da base, infiltração tecidual por corpúsculos de Herring aberrantes, porencefalia e espessamento meníngeo.
5
Brandt, Reynaldo André, João Vitor Salvajoli, Vinio Cintra Oliveira, Marcia Carmignani, José Carlos da Cruz, Heidi Demura Leal et Lygia Ferraz. « [NO TITLE AVAILABLE] ». Arquivos de Neuro-Psiquiatria 53, no 1 (mars 1995) : 38–45. http://dx.doi.org/10.1590/s0004-282x1995000100007.
Texte intégralRésumé :
A radiocirurgia consiste na irradiação precisa de um volume alvo intracraniano com uma alta dose de energia, preservando o tecido nervoso adjacente. O desenvolvimento tecnológico dos aceleradores lineares, dos equipamentos estereotáxicos e da ciência de computação simplificaram o procedimento e tornaram-no acessível. Suas indicações principais são as lesões intracranianas inoperáveis como malformações artério-venosas, schwanomas vestibulares e de outros nervos cranianos, meningeomas da base do crânio, gliomas e metástases cerebrais. Mais recentemente o desenvolvimento da radioterapia estereotáxica fracionada ampliou o espectro" de indicações da radiocirurgia para lesões maiores e adjacentes a estruturas nervosas críticas. Apresentamos a nossa experiência inicial com estas técnicas no tratamento de 31 pacientes. Observamos controle adequado das lesões neoplásicas tratadas e aguardamos o tempo necessário para a observação de resultados nas malformações artério-venosas.
6
Muniz, Xellen Cunha, Jacqueline Garcia Duarte et Rodolfo Duarte Nascimento. « Aspectos histopatológicos das lesões dos nervos periféricos : uma abordagem ao sistema nervoso somático ». Conexão Ciência (Online) 16, no 3 (22 décembre 2021) : 96–129. http://dx.doi.org/10.24862/cco.v16i3.1412.
Texte intégralRésumé :
Introdução: As lesões dos nervos periféricos são pouco frequentes nos traumas dos membros. Elas acometem mais os membros superiores de indivíduos do sexo masculino. Dependendo da gravidade, podem resultar em perda da função motora e/ou sensitiva do membro e dor neuropática. Objetivo: Compilar informações relacionadas às classificações e às alterações histopatológicas de lesões do nervo periférico, com enfoque aos componentes do Sistema Nervoso Somático. Metodologia: Foi realizado um levantamento de artigos na base de dados PubMed, sendo considerados apenas estudos publicados em língua inglesa nos últimos 25 anos (1995-2020). Resultados/Discussão: As lesões dos nervos periféricos são classificadas com base nas alterações histológicas e no grau de acometimento. Em reposta à lesão, alterações intrínsecas e extrínsecas ocorrem, respectivamente, no neurônio e nas células não neuronais presentes no microambiente. Nos neurônios, são ativadas diversas vias moleculares, às quais estão relacionadas com a sobrevivência, regeneração e morte celular. Dentre as células não neuronais, destacam-se as células de Schwann, os macrófagos e os neutrófilos pela capacidade de limpar o microambiente e deixá-lo propício para a regeneração. Nesse contexto, o infiltrado inflamatório, no local da lesão, e no segmento distal do axônio são considerados eventos importantes, respectivamente, para formar a ponte celular e para promover a Degeneração Walleriana. Por outro lado, a presença de mediadores inflamatórios produzidos localmente pode induzir a dor neuropática. Conclusão: Um melhor entendimento dos processos histopatológicos das lesões dos nervos periféricos pode auxiliar os profissionais da saúde no prognóstico e na elaboração de intervenções terapêuticas mais seguras e eficazes no tratamento.
7
Barco-Ríos, John, Jorge Eduardo Duque-Parra et Johanna Alexandra Barco-Cano. « From animal spirits to scientific revolution in Medicine (first part) ». Revista de la Facultad de Medicina 66, no 2 (1 avril 2018) : 233–36. http://dx.doi.org/10.15446/revfacmed.v66n2.62012.
Texte intégralRésumé :
Introducción. En el desarrollo de la medicina, a partir del siglo VI a.C., se planteó una idea filosófica para explicar el funcionamiento del sistema nervioso con base en elementos conocidos como espíritus animales, considerados durante muchos siglos como agentes transmisores de las sensaciones y del movimiento. Este concepto filosófico de base especulativa prevaleció hasta el siglo XVII con sutiles modificaciones, pero después fue superado mediante demostración con los avances logrados en neurofisiología.Discusión. Por tradición dogmática se aceptó durante muchos siglos que a través de los nervios se transmitían espíritus animales que controlaban las acciones corporales. A partir de la Revolución científica tales ideas cambiaron por conceptos mejor elaborados con apoyo del método científico.Conclusión. El concepto que se tenía antiguamente sobre el funcionamiento del sistema nervioso cambió de forma radical a partir del siglo XVII con la ampliación del conocimiento de las características morfofisiológicas de los nervios, abriendo nuevas puertas en busca de explicaciones más coherentes y desligadas de cualquier influencia religiosa.
8
Appenzeller, Simone. « Neuropatias periféricas em doenças autoimunes : abordagem clínica e aspectos terapêuticos ». Revista Paulista de Reumatologia, no 2015 abr-jun;14(2) (30 juin 2015) : 21–24. http://dx.doi.org/10.46833/reumatologiasp.2015.14.2.21-24.
Texte intégralRésumé :
O sistema nervoso é frequentemente acometido nas doenças reumatológicas. Enquanto o comprometimento do sistema nervoso central foi bem caracterizado e investigado, o mesmo não pode ser dito das neuropatias periféricas. Do ponto de vista anatômico, o sistema nervoso periférico pode ser envolvido em qualquer das partes que o compõem, desde a raiz nervosa até as porções mais distais dos ramos terminais dos axônios. Portanto, as neuropatias periféricas podem envolver o corpo celular (neuronopatias) e os processos periféricos (neuropatias periféricas). As neuronopatias podem ser subclassificadas em doenças que comprometem somente o corno anterior (doenças do neurônio motor) e aquelas envolvendo somente neurônios sensitivos (ganglionopatias). Já as neuropatias periféricas podem ser subdivididas em doenças que afetam principalmente a mielina (mielinopatias) e aquelas que afetam os axônios (axoniopatias). Seu acometimento pode estar presente em todas as faixas etárias, sendo maior nas idades mais avançadas, com uma prevalência de 2,4% até 8% ou 10% na população geral. Nas doenças reumatológicas, a prevalência tem sido descrito em 5-15%, mas varia de acordo com a doença de base. A identificação etiológica é fundamental para um tratamento adequado. A anamnese e o exame físico são fundamentais para classificar adequadamente o comprometimento neuropático.
9
Caballero Torres, Angel Eladio, et Yumy Estela Fernández Vélez. « Asociaciones entre alimentos, flora intestinal y sistema nervioso central ». QhaliKay. Revista de Ciencias de la Salud ISSN : 2588-0608 2, no 1 (30 avril 2018) : 35. http://dx.doi.org/10.33936/qkrcs.v2i1.1405.
Texte intégralRésumé :
Existe un incremento del interés sobre posibles efectos de la alimentación en el funcionamiento del sistema nervioso central, aunque la importancia de esa influencia parece requerir mayores respaldos científicos. Estos señalamientos son motivos para valorar, sobre la base de los aportes de otros autores, el posible significado de la relación de alimentos, flora intestinal y sistema nervioso. Para cumplir este objetivo fue necesario una búsqueda de informaciones científicas en la US National Library of Medicine sobre este tema, una selección de publicaciones relevantes y análisis de los datos encontrados. Según esas publicaciones, la protección de la inocuidad de los alimentos, probióticos y algunas sustancias químicas de la dieta tienen relación con la composición y funcionamiento de la flora intestinal que puede afectar el eje intestino cerebro y causar alteraciones en el funcionamiento del sistema nervioso central. Se acepta que son insuficientes las explicaciones sobre relaciones específicas entre componentes de la dieta y efectos en el sistema nervioso central de los consumidores de alimentos, incluyendo los posibles mecanismos de esas relaciones.
Palabras clave: alimentos, eje intestino cerebro, sistema nervioso central, microbiota intestinal.
Abstract
There is an increased interest in possible effects of food on the central nervous system functioning, although the importance of this influence seems to require more scientific support. These indications are reasons to value, based on the contributions of other authors, the possible meaning of the relationship of food with the intestinal flora and the nervous system. To accomplish this goal, a search of scientific information was necessary for the US National Library of Medicine on this topic, a selection of relevant publications and analysis of the data found. According to those publications, food safety, probiotics and some dietary chemicals has a relationship with to the composition and functioning of the intestinal microbiome that can affect the brain intestinal axis and cause alterations in the functioning of the central nervous system. It’s accepted that explanations about specific relationships between diet components and effects on the central nervous system of food consumers, including the possible mechanisms of these relationships, are insufficient.
Key words: food, intestine brain axis, central nervous system, nutrition, intestinal microbiota.
10
Caballero Torres, Angel Eladio, et Yumy Estela Fernández Vélez. « Asociaciones entre alimentos, flora intestinal y sistema nervioso central ». QhaliKay. Revista de Ciencias de la Salud ISSN : 2588-0608 2, no 1 (30 avril 2018) : 35. http://dx.doi.org/10.33936/qhalikay.v2i1.1405.
Texte intégralRésumé :
Existe un incremento del interés sobre posibles efectos de la alimentación en el funcionamiento del sistema nervioso central, aunque la importancia de esa influencia parece requerir mayores respaldos científicos. Estos señalamientos son motivos para valorar, sobre la base de los aportes de otros autores, el posible significado de la relación de alimentos, flora intestinal y sistema nervioso. Para cumplir este objetivo fue necesario una búsqueda de informaciones científicas en la US National Library of Medicine sobre este tema, una selección de publicaciones relevantes y análisis de los datos encontrados. Según esas publicaciones, la protección de la inocuidad de los alimentos, probióticos y algunas sustancias químicas de la dieta tienen relación con la composición y funcionamiento de la flora intestinal que puede afectar el eje intestino cerebro y causar alteraciones en el funcionamiento del sistema nervioso central. Se acepta que son insuficientes las explicaciones sobre relaciones específicas entre componentes de la dieta y efectos en el sistema nervioso central de los consumidores de alimentos, incluyendo los posibles mecanismos de esas relaciones.
Palabras clave: alimentos, eje intestino cerebro, sistema nervioso central, microbiota intestinal.
Abstract
There is an increased interest in possible effects of food on the central nervous system functioning, although the importance of this influence seems to require more scientific support. These indications are reasons to value, based on the contributions of other authors, the possible meaning of the relationship of food with the intestinal flora and the nervous system. To accomplish this goal, a search of scientific information was necessary for the US National Library of Medicine on this topic, a selection of relevant publications and analysis of the data found. According to those publications, food safety, probiotics and some dietary chemicals has a relationship with to the composition and functioning of the intestinal microbiome that can affect the brain intestinal axis and cause alterations in the functioning of the central nervous system. It’s accepted that explanations about specific relationships between diet components and effects on the central nervous system of food consumers, including the possible mechanisms of these relationships, are insufficient.
Key words: food, intestine brain axis, central nervous system, nutrition, intestinal microbiota.
Thèses sur le sujet "Basi nervose"
1
Ng, Tat-fong. « Molecular basis for regeneration of CNS : a possible regulatory role of growth associated protein-43 / ». Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17538786.
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2
吳達方 et Tat-fong Ng. « Molecular basis for regeneration of CNS : a possible regulatory role of growth associated protein-43 ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31235219.
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3
Roshan, Payam. « Cellular basis of inflammation in the enteric nervous system ». Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26759.
Texte intégralRésumé :
There is limited knowledge of immunocyte-myenteric neuronal interaction and the role of iNOS in myenteric neuronal injury. This research sought to examine the role of macrophages, NO, and iNOS inhibitors in myenteric neurodegeneration.
Increased NO synthesis in macrophages and its effects on myenteric neurons were investigated in cell cultures. Using rodent models of inflammation, we further examined NO-dependent neurotoxicity.
In the presence of activated macrophages neuronal injury and degeneration occurred; however the myenteric neurons showed greater resistance to oxidative challenge than cortical neurons. Pretreatment with iNOS inhibitors significantly reduced these inflammatory effects. Myenteric neuronal injury was also evident in experimental colitis, and iNOS selective inhibitor protected the myenteric neurons from inflammation and degeneration.
In conclusion, these results show that activated macrophage-derived NO is important in inflammation-dependent myenteric neurodegeneration, and iNOS inhibitors can protect myenteric neurons from degeneration. Two potential strategies for neuroprotection in gut inflammation are defined.
4
Jaramillo, Martinez Diana. « Epidemiology and pathogenesis of Nervous Necrosis Virus ». Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13088.
Texte intégralRésumé :
Viral Nervous Necrosis (VNN) is a globally distributed disease that affects a large number of finfish species, causing significant economic losses on affected farms. The causative agent is a small single stranded RNA virus called Nervous Necrosis Virus (NNV) from the genus Betanodavirus. NNV is neurotropic; clinical signs involve abnormal behaviour and high mortality associated with histopathological findings of vacuolating necrosis in the central nervous system and retina. In Australia, NNV has been isolated from Australian bass (Macquaria Novemaculeata) and barramundi (Lates calcarifer) populations recurrently for the past 10 and 25 years, respectively. However, the prognosis of NNV infection is highly variable. Although NNV became notorious for mass mortalities in marine fish hatcheries, it is often detected in apparently healthy individuals in the absence of clinical signs or histopathological lesions. Current knowledge on NNV epidemiology and pathogenesis is fragmentary. It is still unclear how the virus is transmitted between hosts and why some individuals are susceptible to VNN while others are not. The aim of this work was to study the epidemiology and pathogenesis of NNV in Australian native species with a focus on transmission and disease determinants to provide a basis for the development of prevention and control strategies. In Chapter 3, a partially retrospective study was conducted on the occurrence of NNV at the Darwin Aquaculture Centre (DAC), a barramundi hatchery. Observations on NNV detection frequency and distribution provided clues to the possible transmission pathways of the virus, including the potential role of broodstock as reservoirs, and the age-dependency of the disease. To assess the NNV exposure distribution among populations of adult fish, an indirect antibody detection ELISA was developed (Chapter 4). The assay was optimized and compared with a competitive ELISA format to provide the best discriminatory power between sera from immunized and non-immunized populations. After defining the best antibody detection protocol (the indirect ELISA), the diagnostic accuracy of the assay was assessed in naturally exposed subjects using a Bayesian approach in the absence of a gold standard (Chapter 5). After validation of the ELISA, a single point and repeated cross sectional analysis of NNV seroprevalence was conducted on native Australian adult fish populations (barramundi, Australian bass and groupers Epinephelus sp.) (Chapter 6). Survey results discredited the role of broodstock as NNV reservoirs based on the lack of correspondence between NNV seroprevalence and the occurrence of NNV outbreaks at the hatchery level. Results also suggested that the exposure of adult fish to NNV antigens must be progressive as seroconversion was often observed and the seroprevalence tended to be higher in older fish populations. From this and previous accumulated epidemiological evidence, horizontal transmission of NNV was considered most likely. An environmental reservoir outside the hatcheries has yet to be investigated. In Chapter 7, the factors influencing the pathogenesis of NNV in barramundi were explored. Juveniles of different ages were challenged by immersion to analyse the influence of the age of the host on VNN disease expression. Additionally, to test the influence of the virus isolate, juveniles were challenged with two inoculums obtained from NNV outbreaks in barramundi populations with different disease presentation (clinical and subclinical). Results showed that fish from all the age groups tested (range 20 to 63 days post hatch) were susceptible to NNV infection. However, the survival of the fish following NNV challenge was highly influenced by the age of the host. Juveniles of 5 weeks of age and older showed no clinical signs and their survival odds were the same as the non-challenged controls, whereas younger fish developed clinical disease. No significant effect on disease severity was noted between different NNV isolates. In Chapter 8, the factors influencing the pathogenesis of NNV in Australian bass were explored. In addition to the age of the host and the isolate factor, the influence of the dose of the virus and the water temperature on VNN expression was examined. As with barramundi, the disease expression in Australian bass was age dependent. The severity of the disease was affected by the water temperature in younger fish but it did not affect the outcome in fish above 5 weeks of age. The dose of the virus influenced the incidence of infection but not the severity of the disease expression. Again, no significant effect on disease severity was noted between the two isolates tested. From the experimental challenge of barramundi and Australian bass, further observations on NNV pathogenesis were provided: incubation period, minimum infectious dose, tissue distribution, shedding and humoral immune response. The results from this study narrow the knowledge gap on NNV transmission mechanisms and provide important insights into the virus pathogenesis in barramundi and Australian bass. The virus is most likely being transmitted horizontally and VNN disease expression as distinct from infection with NNV is highly age dependent. From this evidence, recommendations are made on the direction of efforts to control VNN at the farm level.
5
Caruso, Giuseppe. « Basi Molecolari dei DCP (disoridni conformazionali proteici) a carico del sistema nervoso : condizioni microambientali e interrelazioni cellulari ». Doctoral thesis, Università di Catania, 2014. http://hdl.handle.net/10761/1532.
Texte intégralRésumé :
La funzione biologica di una proteina dipende dalla sua struttura tridimensionale, che è determinata dalla sua sequenza aminoacidica durante il processo di folding proteico. Il folding proteico nella cellula è un processo strettamente regolato che coinvolge una serie di proteine, dai chaperon molecolari alle proteasi, che assistono il processo folding e monitorano la qualità del prodotto finale. Molte malattie hanno mostrato di derivare da misfolding e sono raggruppate sotto il nome di disordini conformazionali proteici (DCP) . L'evento distintivo nei PCD è un cambiamento nella struttura secondaria e/o terziaria di una proteina normale senza alterazione della struttura primaria. Il cambiamento conformazionale può promuovere la malattia aumentando l attività tossica o causando la mancanza di funzione biologica della proteina nativa. I DCP comprendono il morbo di Alzheimer (AD) , il morbo di Huntington (HD), la fibrosi cistica, il diabete mellito di tipo II (T2DM), il morbo di Parkinson (PD), e molte altre malattie. Nella maggior parte dei DCP la proteina mal ripiegata è ricca di strutture beta-sheet. Sia T2DM che AD sono caratterizzati da aggregati proteici insolubili con conformazione fibrillare. L aggregazione dell amilina è associata alla perdita delle cellule beta pancreatiche, mentre Abeta e la formazione grovigli neurofibrillari sono associati alla perdita di cellule neuronali. Sono stati mostrati sia condivisi che separati modelli di tossicità per le due molecole amiloidogeniche Amilina e Abeta, che sono in parte mediati da recettori, con i recettori, almeno in una certa misura, condivisi tra le due molecole. Fattori microambientali quali gli ioni metallici sono noti interagire con queste molecole amiloidogeniche, rendendole tossiche per le cellule in coltura.
Nel presente studio abbiamo dimostrato come i peptidi amiloidogenici formano spontaneamente aggregati amorfi o fibrillari. In presenza di rame la fibrillogenesi di Abeta25 35 subisce delle modifiche strettamente legate al tempo di incubazione, in particolare nel passaggio da una specie all altra. Questi cambiamenti possono essere correlati al grado di tossicità misurato dopo il trattamento di colture cellulari di neuroblastoma (SH-SY5Y). L aumento della tossicità cellulare, indotta mediante incubazione con rame, può essere spiegata con un rallentamento nell evoluzione verso strutture non tossiche, e con la conseguente stabilizzazione di aggregati oligomerici, notoriamente molto più tossici rispetto alle specie fibrillari.
L'incubazione favorisce la formazione di strutture beta-sheet da parte di hA17-29. Lo stato di aggregazione cambia in funzione del tempo di incubazione. La presenza di rame in soluzione rallenta il processo di fibrillogenesi e favorisce la stabilizzazione di specie oligomeriche, mentre altri fattori, quali lo zinco e il ribosio, favoriscono la formazione di grandi aggregati. La vitalità delle cellule di neuroblastoma diminuisce in relazione al tempo di incubazione del frammento peptidico. La pre-incubazione in presenza di rame aumenta ulteriormente la tossicità del peptide. Questa diminuzione della vitalità potrebbe anche dipendere dalla formazione di radicali liberi tossici prodotti come risultato di reazioni di Fenton.
L'analisi del medium condizionato da cellule endoteliali ha mostrato il collegamento fra la produzione di alphaB-cristallina e lo stress cellulare. È stato dimostrato che la produzione di alphaB cristallina è direttamente proporzionale alla concentrazione di peptide Abeta25-35 usato per trattare le colture cellulari. Questo è in accordo con i dati di letteratura in cui l aumentata produzione di HSP, necessarie per il corretto ripiegamento delle proteine e per la protezione delle cellule, è collegata ad eventi di stress cellulare.
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CARUSO, GIUSEPPE. « Basi Molecolari dei DCP (disoridni conformazionali proteici) a carico del sistema nervoso : condizioni microambientali e interrelazioni cellulari ». Doctoral thesis, Università degli studi di Catania, 2014. http://hdl.handle.net/20.500.11769/490585.
Texte intégralRésumé :
La funzione biologica di una proteina dipende dalla sua struttura tridimensionale, che è determinata dalla sua sequenza aminoacidica durante il processo di folding proteico. Il folding proteico nella cellula è un processo strettamente regolato che coinvolge una serie di proteine, dai chaperon molecolari alle proteasi, che assistono il processo folding e monitorano la qualità del prodotto finale. Molte malattie hanno mostrato di derivare da misfolding e sono raggruppate sotto il nome di disordini conformazionali proteici (DCP) . L'evento distintivo nei PCD è un cambiamento nella struttura secondaria e/o terziaria di una proteina normale senza alterazione della struttura primaria. Il cambiamento conformazionale può promuovere la malattia aumentando l’attività tossica o causando la mancanza di funzione biologica della proteina nativa. I DCP comprendono il morbo di Alzheimer (AD) , il morbo di Huntington (HD), la fibrosi cistica, il diabete mellito di tipo II (T2DM), il morbo di Parkinson (PD), e molte altre malattie. Nella maggior parte dei DCP la proteina mal ripiegata è ricca di strutture beta-sheet. Sia T2DM che AD sono caratterizzati da aggregati proteici insolubili con conformazione fibrillare. L’aggregazione dell’amilina è associata alla perdita delle cellule beta pancreatiche, mentre Abeta e la formazione grovigli neurofibrillari sono associati alla perdita di cellule neuronali. Sono stati mostrati sia condivisi che separati modelli di tossicità per le due molecole amiloidogeniche Amilina e Abeta, che sono in parte mediati da recettori, con i recettori, almeno in una certa misura, condivisi tra le due molecole. Fattori microambientali quali gli ioni metallici sono noti interagire con queste molecole amiloidogeniche, rendendole tossiche per le cellule in coltura. Nel presente studio abbiamo dimostrato come i peptidi amiloidogenici formano spontaneamente aggregati amorfi o fibrillari. In presenza di rame la fibrillogenesi di Abeta25 35 subisce delle modifiche strettamente legate al tempo di incubazione, in particolare nel passaggio da una specie all’altra. Questi cambiamenti possono essere correlati al grado di tossicità misurato dopo il trattamento di colture cellulari di neuroblastoma (SH-SY5Y). L’aumento della tossicità cellulare, indotta mediante incubazione con rame, può essere spiegata con un rallentamento nell’evoluzione verso strutture non tossiche, e con la conseguente stabilizzazione di aggregati oligomerici, notoriamente molto più tossici rispetto alle specie fibrillari. L'incubazione favorisce la formazione di strutture beta-sheet da parte di hA17-29. Lo stato di aggregazione cambia in funzione del tempo di incubazione. La presenza di rame in soluzione rallenta il processo di fibrillogenesi e favorisce la stabilizzazione di specie oligomeriche, mentre altri fattori, quali lo zinco e il ribosio, favoriscono la formazione di grandi aggregati. La vitalità delle cellule di neuroblastoma diminuisce in relazione al tempo di incubazione del frammento peptidico. La pre-incubazione in presenza di rame aumenta ulteriormente la tossicità del peptide. Questa diminuzione della vitalità potrebbe anche dipendere dalla formazione di radicali liberi tossici prodotti come risultato di reazioni di Fenton. L'analisi del medium condizionato da cellule endoteliali ha mostrato il collegamento fra la produzione di alphaB-cristallina e lo stress cellulare. È stato dimostrato che la produzione di alphaB cristallina è direttamente proporzionale alla concentrazione di peptide Abeta25-35 usato per trattare le colture cellulari. Questo è in accordo con i dati di letteratura in cui l’aumentata produzione di HSP, necessarie per il corretto ripiegamento delle proteine e per la protezione delle cellule, è collegata ad eventi di stress cellulare.The biological function of a protein depends on its tridimensional structure, which is determined by its amino acid sequence during the process of protein folding. Protein folding in the cell is a tightly regulated process, involving a series of proteins, from molecular chaperones to proteases that assist the folding process and monitor the quality of the final product. Several diseases have been shown to arise from protein misfolding and are grouped together under the name of protein conformational disorders (PCDs). The hallmark event in PCDs is a change in the secondary and/or tertiary structure of a normal protein without alteration of the primary structure. The conformational change may promote the disease by either gain of a toxic activity or by the lack of biological function of the natively folded protein. The PCDs includes Alzheimer's disease (AD), Huntington disease (HD), cystic fibrosis, diabetes mellitus type II (T2DM), Parkinson disease (PD), and many other diseases. In most of PCDs the misfolded protein is rich in beta-sheet conformation. Both T2DM and AD are characterized by insoluble protein aggregates with a fibrillar conformation. Amylin aggregation is associated with pancreatic beta-cell loss, whereas Abeta and tangle formation is associated with neuronal cell loss. For the two amyloidogenic molecules Amylin and Abeta, shared and separate modes of toxicity have been revealed, that are in part receptor-mediated, with the receptors, at least to some degree, being shared between the two molecules. Microenvironmental factors such as metal ions are known to interact with these amyloidogenic molecules, and make them toxic for cultured cells. In the present study, we show that amyloidogenic peptides spontaneously form amorphous or fibrillary aggregates. In presence of copper Abeta25 35 fibrillogenesis undergoes changes, tightly linked to the time of incubation, especially in the shift from one species to another. These changes may be related to the toxicity degree measured after treatment of neuroblastoma cell cultures (SH-SY5Y). Cellular toxicity increase, induced by incubation with copper, may be explained with a slowdown in the evolution toward not toxic structures, and a consequent stabilization of oligomeric aggregates, notoriously much more toxic than fibrillary species. The incubation favors the formation of beta-sheet structures by hA17-29. The state of aggregation changes as a function of incubation time. The presence of copper in solution slows the fibrillogenesis process, and favors the stabilization of oligomeric species, instead other factors such as zinc and ribose favor the formation of large aggregates. The neuroblastoma cells viability decreases in relation to incubation time of the peptide fragment. The pre-incubation in the presence of copper further increases the toxicity of the peptide. This decrease of viability could also depend on the formation of toxic free radical species produced as a result of Fenton reactions. The analysis of the conditioned medium from endothelial cells shown a connection between alphaB-cristallin production and cellular stress. The production of alphaB-crystallin has been shown directly proportional to the concentration of Abeta25-35 peptide used to treat cell cultures. This is in agreement with literature data in which increased production of HSP, necessary for the proper folding of proteins and for the cell protection, is connected to events of cellular stress.
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Lloyd, Edward John, et mikewood@deakin edu au. « A common structural basis for central nervous system drug design ». Deakin University. School of Biological Sciences, 1986. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050902.115505.
Texte intégralRésumé :
The main theme of this thesis is that there is a common structural basis for drugs acting on the central nervous system (CNS), and that this concept may be used to design new CNS-active drugs which have greater specificity and hence less side-effects.
To develop these ideas, the biological basis of how drugs modify CMS neurotransmission is described, and illustrated using dopaminergic pathways. An account is then given of the use of physicochemical concepts in contemporary drug design. The complete conformational analysis of several antipsychotic drugs is used to illustrate some of these techniques in the development of a model for antipsychotic drug action.
After reviewing current structure-activity studies in several classes of CNS drugs (antipsychotics, anti-depressants, stimulants, hal1ucinogens, anticonvulsants and analgesics), a hypothesis for a common structural basis of CNS drug action is proposed- This is based on a topographical comparison of the X-ray structures of eight representative CNS-active drugs, and consists of three parts: 1.there is a common structural basis for the activity of many different CNS-active drug classes; 2. an aromatic ring and a nitrogen atom are the primary binding groups whose topographical arrangement is fundamental to the activity of these drug classes;
3. the nature and placement of secondary binding
determines different classes of CNS drug activity. A four-Point model for this common structural basis is then defined using 14- CNS-active drug structures that include the original eight used in proposing the hypothesis. The coordinates of this model are: R1 (0. 3.5, 0), R2 (0, -3.5, O), N (4.8. -0.3, 1.4), and R3 (6.3, 1.3, 0), where R1 and R2 represent the point locations of a hydrophobic interaction of the common aromatic ring with a receptor, and R3 locates the receptor point for a hydrogen bond involving the common nitrogen, N. Extended structures were used to define the receptor points R1, R2 and R3, and the complete conformational space of each of the 14 molecules was considered.
It is then shoun that the model may be used to predict whether a given structure is likely to show CNS activity: a search over 1,000 entries in the current Merck Index shows a high probability (82%) of CNS activity in compounds fitting the structural model.
Analysis of CNS neurotransmitters and neuropeptides shows that these fit the common model well. Based on the available evidence supporting chemical evolution, protein evolution, and the evolution of neurotransmitter functions, it is surmised that the aromatic ring/nitrogen atom pharmacophore proposed in the common model supports the idea of the evolution of CNS receptors and their neurotransmitters, possibly from an aromatic amine or acety1cho1ine acting as a primaeval communicating molecule.
The third point in the hypothesis trilogy is then addressed. The extensive conformation-activity analyses that have resulted in well-defined models for five separate CNS drug classes are used to map out the locations of secondary binding groups relative to the common model for anti-psychotics, antidepressants, analgesics, anticholinergics, and anticonvulsants. With this information, and knowledge derived from receptor-binding data, it is postulated that drugs having specified activity could be designed.
In order to generate novel structures having a high probability of CNS-activity, a process of drug design is described in which known CNS structures are superimposed topographically using the common model as a template. Atoms regarded as superfluous may be selectively deleted and the required secondary binding groups added in predicted locations to give novel structures.
It is concluded that this process provides the basis for the rational design of new lead compounds which could further be optimized for potent and specific CNS activity.
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Shi, Huilin. « The common basis of sympathetic nervous system and neuroblastoma development ». Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1244058100.
Texte intégralRésumé :
Thesis (Ph. D.)--University of Toledo, 2009."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences (Cancer Biology)." Title at OhioLINK ETD site: Investigation of common bases of sympathetic nervous system and neuroblastoma development. Title from title page of PDF document. Includes bibliographical references (p. 72-75, 119-125, 152-192).
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Nazer, Manoel Brandes. « Sistematização das artérias da base do encéfalo de avestruz (struthio camelus) ». reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/16335.
Texte intégralRésumé :
O avestruz (Struthio camelus) é uma ave da família Struthionidae, originária da África. Embora a irrigação da base do encéfalo de outras aves já tenha sido fonte de estudo por alguns pesquisadores, desconhece-se o padrão, as variações, as distribuições e o comportamento das artérias que promovem a irrigação sangüínea na base do encéfalo em avestruz. Neste trabalho, foram utilizados 30 espécimes, nos quais o sistema arterial foi preenchido com látex corado em vermelho através das artérias (Aa.) carótida comum direita e esquerda. Sistematizou-se as artérias da face ventral do encéfalo, à direita e à esquerda, com suas respectivas percentagens de ocorrência. A a. carótida do cérebro, um vaso de grosso calibre, foi predominante na direita (43,3%), esquerda (36,7%) e equivalentes (20%). A anastomose intercarótica apresentou calibre médio (46,7%), grosso (43,3%) e fino (10%), tendo inclinação de fluxo para esquerda (53,3%) e direita (46,7%). A a. oftálmica interna direita apresentou, à direita, calibre médio (43,3%), fino (33,3%) e grosso (23,3%); à esquerda, calibre médio (60%), fino (26,7%) e grosso (13,3%). O ramo caudal da a. carótida do cérebro foi, á direita, desenvolvido (53,3%) e vestigial (46,7%); à esquerda, desenvolvido (66,7%) e vestigial (33,3%). A a. tectal mesencefálica ventral foi ramo colateral do ramo caudal da a. carótida do cérebro à direita (53,3%) e à esquerda (66,7%), ramo direto da a. carótida do cérebro à direita (43,3%) e à esquerda (30%) e, ramo direto da a. basilar (3,3%) em ambos os antímeros. A a. basilar foi um vaso ímpar (80%), duplo em quase toda sua extensão calibrosa (13,3%) e, apresentou uma formação "em ilha" em seu segmento de grosso calibre (6,7%). A a. cerebelar ventral caudal foi única (96,7%) e dupla (3,3%) à direita e, única (93,3%) e dupla (6,7%) à esquerda. A a. espinhal dorsal foi ramo colateral da a. cerebelar ventral caudal à direita (96,7%) e à esquerda (93,3%), sendo também ramo da porção fina da a. basilar à direita (3,3%) e à esquerda (6,7%). A a. espinhal ventral, sempre ramo da a. basilar, foi dupla (90%) e única (10%). O ramo rostral da a. carótida do cérebro, um vaso de grosso calibre, apresentou, à direita, um trajeto padrão (86,7%) e um deslocamento rostral (13,3%) e, à esquerda, trajeto padrão (83,3%) e um deslocamento rostral (16,7%). A a. cerebral caudal, à direita, foi dupla (90%) e única (10%); à esquerda, foi dupla (53,3%) e única (46,7%). A a. cerebral média, em ambos os antímeros, foi um vaso único (100%) e de grosso calibre, sendo o segundo ramo colateral do ramo rostral da a. carótida do cérebro. A a. cerebroetmoidal foi única (100%), de médio a grosso calibre, em ambos os antímeros. A a. cerebral rostral foi única (90%) e dupla (10%) à direita e única (96,7%) e dupla (3,3%) à esquerda. A a. etmoidal foi única (100%), de médio a grosso calibre, sendo a continuação natural da a. cerebroetmoidal, após a emissão da a. cerebral rostral. O círculo arterial cerebral apresentou-se rostralmente aberto (100%) e, caudalmente, aberto (80%) e fechado (20%).The ostrich (Struthio camelus) is a bird from the Struthionidae family, originated from Africa. Although the irrigation of the base of the brain of other birds has already been the source of study by some researchers, the pattern, variations, distribution and the behavior of the arteries that promote the blood irrigation in the base of ostrich's brain are not known. In this work, 30 specimens, in which the arterial system was filled with red colored latex in the common carotid arteries left and right. We systematized the arteries of the ventral face of the brain, to the right and to the left, with their respective occurrence percentage. The carotid artery (a.) of the brain, a thick caliber vase, was predominant in the right (43.3%), left (36.7%) and equivalents (20%). The intercarotid anastomosis presented a medium caliber (46.7%), thick (43.3%) and thin (10%), with flux inclination to the left (53.3%) and right (46.7%). The inner right ophthalmic a. presented, to the right, medium caliber (43.3%), thin (33.3%) and thick (23.3%); to the left, medium caliber (60%), thin (26.7%) and thick (13.3%). The caudal branch of the carotid a. of the brain was, to the right, developed (53.3%) and vestigial (33.3%). The midbrain ventral tectal a. was the collateral branch of the caudal branch of the carotid a. of the brain to the right (53.3%) and to the left (66.7%), right branch of the carotid a. of the brain to the right (43.3%) and to the left (30%) and, right branch of the basilar a. (3.3%) in both antimeres. The basilar a. was an unpaired vase (80%), double in almost the entire caliber extension (13.3%) and, presented the "island" formation in its segment of thick caliber (6.7%). The caudal ventral cerebellar a. was single (96.7%) and double (3.3% to the right and, single (93.3%) and double (6.7%) to the left. The dorsal spinal a. was a collateral branch of the caudal ventral cerebellar a. to the right (96.7%) and to the left (93.3%), which was also a branch of the thin portion of the basilar a. to the right (3.3%) and to the left (6.7%). The ventral spinal a., always a branch of the basilar a., was double (90%) and single (10%). The rostral branch of the carotid a. of the brain, a vase of thick caliber, presented, to the right, a standard path (86.7%) and a rostral displacement (13.3%) and, to the left, a standard path (83.3%) and a rostral displacement (16.7%). The caudal brain a., to the right, was double (90%) and single (10%); to the left, it was double (53.3%) and single (46.7%). The medium cerebral a., in both antimeres, was a single vase (100%) and of thick caliber, being that the second collateral branch of the rostal branch of the brain carotid a. The brain ethmoidal a. foi single (100%), of medium to thick caliber, in both antimeres. The rostral brain a. was single (90%) and double (10%) to the right and single (96.7%) and double (3.3%) to the left. The ethmoidal a. was single (100%), of medium to thick caliber, being the natural continuity of the brain ethmoidal, after the emission of the rostral brain a.. The brain artery circle was rostrally open (100%) and, caudally, open (80%) and closed (20%).
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Hayden, James Timothy. « The molecular basis for central nervous system primitive neuroectodermal tumour development ». Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1598.
Texte intégralRésumé :
Central nervous system primitive neuroectodermal tumours (CNS-PNETs) are highly aggressive tumours with similar histopathological features to other intracranial PNETs (medulloblastomas). These two tumours have accordingly been treated using unified approaches, but CNS-PNETs have a dismal prognosis. Few studies have investigated the genetic features of CNS-PNETs. The molecular basis of CNS-PNET was therefore investigated in a cohort containing CNS-PNETs from children (n=33) and adults (n=5), to aid improvements in disease classification and treatment. The common medulloblastoma molecular defects were investigated in CNS-PNETs, and showed RASSF1A promoter hypermethylation is a frequent event (18/22, 82%), and MYC family gene amplification occurs in a subgroup (MYCN: 3/25 (12%), MYCC: 0/25 (0%)). In contrast and in distinction to medulloblastoma, chromosome 17p loss is not a common feature (2/23, 9%), whilst p53 pathway signalling appears to play a major role (20/22, 91%), and associated with TP53 mutations (4/22, 18%). Aberrant Wnt signalling was identified in 2 cases (2/22, 9%) and coupled with CTNNB1 mutation in a single case. IDH1 mutations (2/25, 8%) however, appear to occur in adult but not childhood CNS-PNETs or medulloblastoma. Subsequent genome-wide investigations of the CNS-PNET DNA methylome aimed at a wider characterisation of the molecular features of CNS-PNETs and its relationships to other childhood tumours identified CNS-PNETs as a heterogenous disease group without defined sub-clusters, which were predominantly distinct from medulloblastomas, but exhibited overlap with high-grade gliomas. A panel of 76 tumour-specific methylation events were identified as disease markers. The combination of either RASSF1A hypermethylation or HLA-DPB1 hypomethylation discerned normal brain from CNS-PNET in 94% of cases (64/68). In addition, hypermethylation of TAL1, MAP3K1 and IGFBP1 is associated with non-infant disease. In conclusion, this study has shown CNS-PNETs are a heterogenous group of tumours that are molecularly distinct from medulloblastomas, and has implicated developmental pathways and genetic events in their tumorigenesis. The associations between molecular events identified and clinical features warrant further investigation to aid classification and treatment advancements.
Livres sur le sujet "Basi nervose"
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H, Tuszynski Mark, et Kordower Jeffrey H, dir. CNS regeneration : Basic science and clinical advances. San Diego : Academic Press, 1999.
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M, Fichter Manfred, dir. Bulimia nervosa : Basic research, diagnosis, and therapy. Chichester : Wiley, 1990.
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Basic neurology. 2e éd. New York : Pergamon Press, 1990.
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Basic neurology. 3e éd. New York : McGraw-Hill, 2000.
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1950-, Young Paul H., dir. Basic clinical neuroanatomy. Baltimore : Williams & Wilkins, 1997.
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Manual of basic neuropathology. 3e éd. Philadelphia : Saunders, 1990.
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1950-, Young Paul H., Tolbert Daniel L. 1946- et Young Paul A. 1926-, dir. Basic clinical neuroscience. 2e éd. Philadelphia : Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.
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Benarroch, Eduardo E. Basic neurosciences with clinical applications. Philadelphia : Butterworth Heinemann/Elsevier, 2006.
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Smith, Carlton G. Basic neuroanatomy. 3e éd. Lexington, Mass : Collamore Press, 1985.
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Brumback, Roger A. Neuropathology and basic neuroscience. New York : Springer-Verlag, 1995.
Trouver le texte intégralChapitres de livres sur le sujet "Basi nervose"
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Crow, Scott J., et Elke D. Eckert. « Anorexia Nervosa and Bulimia Nervosa ». Dans The Medical Basis of Psychiatry, 211–28. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2528-5_12.
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Nieuwenhuys, Rudolf, Jan Voogd, Christiaan van Huijzen et Michele Papa. « Telencefalo : gangli della base ». Dans Il sistema nervoso centrale, 427–89. Milano : Springer Milan, 2010. http://dx.doi.org/10.1007/978-88-470-1140-3_14.
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Beyzadeoglu, Murat, Gokhan Ozyigit et Cuneyt Ebruli. « Central Nervous System Tumors ». Dans Basic Radiation Oncology, 175–203. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11666-7_4.
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Beyzadeoglu, Murat, Gokhan Ozyigit et Cüneyt Ebruli. « Central Nervous System Tumors ». Dans Basic Radiation Oncology, 123–57. Cham : Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87308-0_4.
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Brown, Ronald T., David O. Antonuccio, George J. DuPaul, Mary A. Fristad, Cheryl A. King, Laurel K. Leslie, Gabriele S. McCormick, William E. Pelham, John C. Piacentini et Benedetto Vitiello. « Anorexia nervosa and bulimia nervosa. » Dans Childhood mental health disorders : Evidence base and contextual factors for psychosocial, psychopharmacological, and combined interventions., 113–19. Washington : American Psychological Association, 2008. http://dx.doi.org/10.1037/11638-011.
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Kryzhanovsky, G. N. « Basic therapeutic principles ». Dans Central Nervous System Pathology, 239–311. Boston, MA : Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-7870-9_13.
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Strominger, Norman L., Robert J. Demarest et Lois B. Laemle. « Basic Neurophysiology ». Dans Noback's Human Nervous System, Seventh Edition, 39–71. Totowa, NJ : Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-779-8_3.
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Tom, Michael, et Thomas M. Halaszynski. « Peripheral Nerve Blocks ». Dans Basic Clinical Anesthesia, 233–51. New York, NY : Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1737-2_22.
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Mountz, James M. « Central Nervous System ». Dans The Pathophysiologic Basis of Nuclear Medicine, 445–524. Cham : Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-96252-4_11.
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Brien, Sarah. « The Biological Basis of Bulimia Nervosa ». Dans Addictive Behaviour : Molecules to Mankind, 191–212. London : Palgrave Macmillan UK, 1996. http://dx.doi.org/10.1007/978-1-349-24657-1_12.
Texte intégralActes de conférences sur le sujet "Basi nervose"
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Spolador, Maria Eduarda Granucci, Heloisa Geovana Guedes et Lucia de Fatima Amorim. « PARASITOSE OPORTUNISTA CAUSADA PELO Toxoplasma gondii EM PACIENTES COM HIV : UMA REVISÃO BIBLIOGRÁFICA. » Dans I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/910.
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Introdução: O Vírus da Imunodeficiência Humana (HIV) é o causador da Síndrome da Imunodeficiência Adquirida (SIDA), o qual infecta primordialmente os linfócitos TCD4, causando um quadro de imunossupressão. Esta, proporciona uma maior suscetibilidade à Toxoplasmose, doença causada pelo Toxoplasma gondii (Nicolle & Manceaux, 1908), desencadeando intercorrências clínicas graves. Essa parasitose apresenta-se como a mais frequente infecção oportunista que afeta o sistema nervoso central (Neurotoxoplasmose) desses imunocomprometidos, visto a capacidade de o HIV reativar a infecção latente pelo T. gondii, configurando-se como uma grande preocupação de saúde pública mundial. Objetivo: Descrever a ação oportunista do T. gondii em indivíduos com SIDA e a sua capacidade de complicações severas com base na literatura. Material e métodos: Realizou-se uma revisão bibliográfica sobre o tema baseada em artigos científicos indexados no PubMed, Scielo e MEDLINE. Resultados: A parasitose oportunista causada pelo T. gondii, parasita intracelular obrigatório, está presente em grande parte dos indivíduos acometidos pela SIDA, com prevalência em países tropicais, como o Brasil. A literatura relata que as manifestações clínicas mais graves originam-se de quadros de Neurotoxoplasmose, atacando células nervosas e provocando lesões multifocais na área frontoparietal, ou no gânglio basal e cerebelo, podendo ocasionar hemiparesia, cefaléia, confusão mental, letargia e convulsões, somado à paralisia de nervos cranianos, acidentes vasculares encefálicos e irritação meníngea. Além da reativação da doença no sistema nervoso central, há ocorrências no pulmão, miocárdio, retina ocular, ou de modo disseminado. Dessa forma, os quadros clínicos apresentados pela coinfecção HIV/T. gondii são altamente graves, com risco de morbimortalidade. Conclusão: Nesse viés, é imprescindível o seguimento dos Protocolos Clínicos e Diretrizes Terapêuticas para o manejo da infecção pelo HIV e suas possíveis coinfecções, como a Toxoplasmose, melhorando a qualidade de vida desses pacientes e evitando possíveis complicações.
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Rogers, Garrett, Noga Lipschitz, Gavriel Kohlberg, Mario Zuccarello et Ravi Sami. « Primary Central Nervous System Lymphoma of the Internal Auditory Canal Mimicking Facial Nerve Schwannoma ». Dans 29th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679739.
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Son, Esther Y., Ahmed Mohyeldin, Arjun Pendharkar, Juan C. Fernandez-Miranda et Andrea L. Kossler. « First Case Report of Primary Central Nervous System Amyloidoma Involving Cranial Nerves V and VII ». Dans Special Virtual Symposium of the North American Skull Base Society. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725557.
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Yazawa, Toru, Yukio Shimoda, Satoru Shimizu et Tomoo Katsuyama. « Neurodynamical Control of the Heart of Freely Moving Animals Including Humans ». Dans ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-85872.
Texte intégralRésumé :
Two kinds of nerves, acceleratory and inhibitory cardio-regulator nerves, innervate the heart. They are known to discharge concurrently to maintain an equilibrium state of the body. The nerves are also known to change their frequency of discharge in a reflexive manner to meet the demand from the periphery; such as augmentation of oxygen supply or vice versa. Consequently, the heart exhibits dynamic change in its pumping rate and force of contraction. If the control system fails, the heart exhibits unhealthy state. However, assessment of healthy/unhealthy status is uneasy because we are not able to monitor the nerve activities by non-invasive methods. Therefore, we challenged to detect state of the heart without nerve-recordings. We used the detrended fluctuation analysis (DFA) applying to heartbeat interval time series because DFA has been believed that it can quantify the state of heart. We performed DFA on the EKGs (electrocardiograms) from various living organisms including humans. The objective of this research was to determine whether the analytical technology, DFA, could function as a useful method for the evaluation of the subject’s quality of cardiovascular-related illness and transition to and from a normal healthy state. We found that DFA could describe brain-heart interaction quantitatively: the scaling exponents of (1) healthy, (2) sick-type (such as stressful or arrhythmic states), and (3) unpredictable-death type (such as ischemic heart disease) were corresponded to individuals who exhibited, (1) nearly one, (2) less than one, and (3) greater than one, respectively. We conclude that scaling exponents could determine whether the subjects are under sick or healthy conditions on the basis of cardiac physiology.
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Barbalho, Caio Henrique Silveira, et Eclésio Batista Oliveira Neto. « NAEGLERIA FOWLERI E A MENINGOENCEFALITE AMEBIANA PRIMÁRIA : TRATAMENTO ». Dans I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/28.
Texte intégralRésumé :
Introdução: A Naegleria fowleri é um protozoário de vida livre, flagelado e termofílo, popularmente conhecido como ameba "comedora de cérebro", é o agente etiológico de uma doença da meningoencefalite amebiana primária (MAP). Uma doença que normalmente afeta jovens adultos, e tem 95-99% de taxa de mortalidade. Objetivo: Revisar a MAP causada por N. fowleri. Material e métodos: Foi realizada uma revisão bibliográfica na base de dados BVS (Biblioteca Virtual em Saúde) e PUBMED com a seguinte combinação de descritores: "Central Nervous System Protozoal Infections" AND "Naegleria fowleri”. Foi definido os seguintes critérios de inclusão: textos condizentes com os objetivos e tema; em português e inglês; e publicados nos últimos 5 anos. A busca retornou 19 artigos, após a aplicação dos critérios de inclusão, foram mantidos e analisados 11 artigos. Resultados: Os artigos revisados enfatizam que o N. fowleri é morfologicamente dividido em: cisto, trofozoíto e flagelados, sendo a trofozoíta. O ciclo de vida do geralmente acontece em ambientes aquáticos, quentes e ricos em nutrientes, eles podem ser encontrados em solos, piscinas e esgotos. No entanto, podem se tornar patogênicos em seres humanos, ao penetrar na mucosa nasal e migrar para o cérebro através do nervo olfatório, então, alcançam a membrana aracnóide, espalhandose pelo sistema nervoso central, levando o paciente ao óbito. O período de incubação ocorre entre 2 a 3 dias ou 7 a 15 dias. Os sintomas são caracterizados por encefalite, cefaleia bifrontal, febre, náuseas e êmese. Às vezes, no início da progressão da doença, parosmia e ageusia ocorrem à medida que os trofozoítos danificam o sistema olfatório. Embora alguns medicamentos empregados no tratamento de AMP como: Anfotericina B, Miltefosina, Rifampicina, mostrem resultados positivos, é difícil afirmar se a doença está sendo tratada corretamente usando uma determinada combinação deles. Conclusão: A MAP é uma doença emergente e infelizmente negligenciada, faz-se necessário mais estudos para melhor proceder com o diagnóstico e desenvolver fármacos mais eficientes e específicos para esta doença.
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Rotter, Juliana, Victor M. Lu, Avital Perry, Christopher S. Graffeo, Matthew L. Carlson, Colin L. Driscoll et Michael J. Link. « Surgery versus Radiosurgery for Facial Nerve Schwannoma : Systematic Review and Meta-analysis of Facial Nerve Function ». Dans 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702363.
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Appelbaum, Eric N., Nathan R. Lindquist et Alex D. Sweeney. « Malignant Peripheral Nerve Sheath Tumor of the Intratemporal Facial Nerve : A First Case Report and Review of the Literature ». Dans 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702640.
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North, Monique, Jeffrey Weishaar et John P. Leonetti. « Intraoperative Electrical Stimulation for Traumatic Facial Nerve Paralysis ». Dans 31st Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1743916.
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Jackson, Neal M., Anna K. Bareiss et Erika M. Moxley. « A Rare Case of Bilateral Facial Nerve Lesions ». Dans 31st Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1743996.
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Gilder, Hannah, Avital Perry, Christopher Graffeo et Michael Link. « Neurosarcoid Presenting with Synchronous Trochlear and Vagus Nerve Palsies ». Dans 29th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679697.
Texte intégralRapports d'organisations sur le sujet "Basi nervose"
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Hillestad, Torgeir Martin. The Metapsychology of Evil : Main Theoretical Perspectives Causes, Consequences and Critique. University of Stavanger, 2014. http://dx.doi.org/10.31265/usps.224.
Texte intégralRésumé :
The purpose of this text or dissertation is to throw some basic light on a fundamental problem concerning manhood, namely the question of evil, its main sources, dynamics and importance for human attitudes and behaviour. The perspective behind the analysis itself is that of psychology. Somebody, or many, may feel at bit nervous by the word “evil” itself. It may very well be seen as too connected to religion, myth and even superstition. Yet those who are motivated to lose oneself in the subject retain a deep interest in human destructiveness, malevolence and hate, significant themes pointing at threatening prospects for mankind. The text is organized or divided into four main ordinary chapters, the three first of them organized or divided into continuous and numbered sections. A crucial point or question is of cause how to define evil itself. It can of cause be done both intentional, instrumental and by consequence. Other theorists however have stated that the concept of evil exclusively rests on a myth originated in the Judean-Christian conception of Satan and ultimate evil. This last argument presupposes evil itself as non-existent in the real rational world. It seems however a fact that most people attach certain basic meaning to the concept, mainly that it represents ultimately bad and terrible actions and behaviour directed toward common people for the purpose of bringing upon them ultimate pain and suffer. However, there is no room for essentialism here, meaning that we simply can look “inside” some original matter to get to know what it “really” is. Rather, a phenomenon gets its identity from the constituted meaning operating within a certain human communities and contexts loaded with intentionality and inter-subjective meaning. As mentioned above, the concept of evil can be interpreted both instrumental and intentional, the first being the broadest of them. Here evil stands for behaviour and human deeds having terrifying or fatal consequences for subjects and people or in general, regardless of the intentions behind. The intentional interpretation however, links the concept to certain predispositions, characteristics and even strong motives in subjects, groups and sometimes political systems and nations. I will keep in mind and clear the way for both these perspectives for the discussion in prospect. This essay represents a psychological perspective on evil, but makes it clear that a more or less complete account of such a psychological view also should include a thorough understanding or integration of some basic social and even biological assumptions. However, I consider a social psychological position of significant importance, especially because in my opinion it represents some sort of coordination of knowledge and theoretical perspectives inherent in the subject or problem itself, the main task here being to integrate perspectives of a psychological as well as social and biological kind. Since humans are essential social creatures, the way itself to present knowledge concerning the human condition, must be social of some sort and kind, however not referring to some kind of reductionism where social models of explanation possess or holds monopoly. Social and social psychological perspectives itself represents parts of the whole matter regarding understanding and explanation of human evil. The fact that humans present, or has to represent themselves as humans among other humans, means that basically a social language is required both to explain and describe human manners and ways of being. This then truly represents its own way or, more correctly, level or standard of explanation, which makes social psychology some sort of significant, though not sufficient. More substantial, the vision itself of integrating different ontological and theoretical levels and objects of science for the purpose of manifesting or make real a full-fledged psychological perspective on evil, should be considered or characterized a meta-psychological perspective. The text is partially constructed as a review of existing theories and theorists concerning the matter of evil and logically associated themes such as violence, mass murder, genocide, antisocial behaviour in general, aggression, hate and cruelty. However, the demands of making a theoretical distinction between these themes, although connected, is stressed. Above all, an integral perspective combining different scientific disciplines is aimed at.
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Altstein, Miriam, et Ronald Nachman. Rationally designed insect neuropeptide agonists and antagonists : application for the characterization of the pyrokinin/Pban mechanisms of action in insects. United States Department of Agriculture, octobre 2006. http://dx.doi.org/10.32747/2006.7587235.bard.
Texte intégralRésumé :
The general objective of this BARD project focused on rationally designed insect neuropeptide (NP) agonists and antagonists, their application for the characterization of the mechanisms of action of the pyrokinin/PBAN (PK-PBAN) family and the development of biostable, bioavailable versions that can provide the basis for development of novel, environmentally-friendly pest insect control agents. The specific objectives of the study, as originally proposed, were to: (i) Test stimulatory potencies of rationally designed backbone cyclic (BBC) peptides on pheromonotropic, melanotropic, myotropic and pupariation activities; (ii) Test the inhibitory potencies of the BBC compounds on the above activities evoked either by synthetic peptides (PBAN, LPK, myotropin and pheromonotropin) or by the natural endogenous mechanism; (iii) Determine the bioavailability of the most potent BBC compounds that will be found in (ii); (iv) Design, synthesize and examine novel PK/PBAN analogs with enhanced bioavailability and receptor binding; (v) Design and synthesize ‘magic bullet’ analogs and examine their ability to selectively kill cells expressing the PK/PBAN receptor. To achieve these goals the agonistic and antagonistic activities/properties of rationally designed linear and BBC neuropeptide (NP) were thoroughly studied and the information obtained was further used for the design and synthesis of improved compounds toward the design of an insecticide prototype. The study revealed important information on the structure activity relationship (SAR) of agonistic/antagonistic peptides, including definitive identification of the orientation of the Pro residue as trans for agonist activity in 4 PK/PBANbioassays (pheromonotropic, pupariation, melanotropic, & hindgut contractile) and a PK-related CAP₂b bioassay (diuretic); indications that led to the identification of a novel scaffold to develop biostbiostable, bioavailable peptidomimetic PK/PBANagonists/antagonists. The work led to the development of an arsenal of PK/PBAN antagonists with a variety of selectivity profiles; whether between different PKbioassays, or within the same bioassay between different natural elicitors. Examples include selective and non-selective BBC and novel amphiphilic PK pheromonotropic and melanotropic antagonists some of which are capable of penetrating the moth cuticle in efficacious quantities. One of the latter analog group demonstrated unprecedented versatility in its ability to antagonize a broad spectrum of pheromonotropic elicitors. A novel, transPro mimetic motif was proposed & used to develop a strong, selective PK agonist of the melanotropic bioassay in moths. The first antagonist (pure) of PK-related CAP₂b diuresis in flies was developed using a cisPro mimetic motif; an indication that while a transPro orientation is associated with receptor agonism, a cisPro orientation is linked with an antagonist interaction. A novel, biostablePK analog, incorporating β-amino acids at key peptidase-susceptible sites, exhibited in vivo pheromonotropic activity that by far exceeded that of PBAN when applied topically. Direct analysis of neural tissue by state-of-the-art MALDI-TOF/TOF mass spectrometry was used to identify specific PK/PK-related peptides native to eight arthropod pest species [house (M. domestica), stable (S. calcitrans), horn (H. irritans) & flesh (N. bullata) flies; Southern cattle fever tick (B. microplus), European tick (I. ricinus), yellow fever mosquito (A. aegypti), & Southern Green Stink Bug (N. viridula)]; including the unprecedented identification of mass-identical Leu/Ile residues and the first identification of NPs from a tick or the CNS of Hemiptera. Evidence was obtained for the selection of Neb-PK-2 as the primary pupariation factor of the flesh fly (N. bullata) among native PK/PK-related candidates. The peptidomic techniques were also used to map the location of PK/PK-related NP in the nervous system of the model fly D. melanogaster. Knowledge of specific PK sequences can aid in the future design of species specific (or non-specific) NP agonists/antagonists. In addition, the study led to the first cloning of a PK/PBAN receptor from insect larvae (S. littoralis), providing the basis for SAR analysis for the future design of 2ⁿᵈgeneration selective and/or nonselective agonists/antagonists. Development of a microplate ligand binding assay using the PK/PBAN pheromone gland receptor was also carried out. The assay will enable screening, including high throughput, of various libraries (chemical, molecular & natural product) for the discovery of receptor specific agonists/antagonists. In summary, the body of work achieves several key milestones and brings us significantly closer to the development of novel, environmentally friendly pest insect management agents based on insect PK/PBANNPs capable of disrupting critical NP-regulated functions.
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Halker Singh, Rashmi B., Juliana H. VanderPluym, Allison S. Morrow, Meritxell Urtecho, Tarek Nayfeh, Victor D. Torres Roldan, Magdoleen H. Farah et al. Acute Treatments for Episodic Migraine. Agency for Healthcare Research and Quality (AHRQ), décembre 2020. http://dx.doi.org/10.23970/ahrqepccer239.
Texte intégralRésumé :
Objectives. To evaluate the effectiveness and comparative effectiveness of pharmacologic and nonpharmacologic therapies for the acute treatment of episodic migraine in adults. Data sources. MEDLINE®, Embase®, Cochrane Central Registrar of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO®, Scopus, and various grey literature sources from database inception to July 24, 2020. Comparative effectiveness evidence about triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) was extracted from existing systematic reviews. Review methods. We included randomized controlled trials (RCTs) and comparative observational studies that enrolled adults who received an intervention to acutely treat episodic migraine. Pairs of independent reviewers selected and appraised studies. Results. Data on triptans were derived from 186 RCTs summarized in nine systematic reviews (101,276 patients; most studied was sumatriptan, followed by zolmitriptan, eletriptan, naratriptan, almotriptan, rizatriptan, and frovatriptan). Compared with placebo, triptans resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (high strength of the body of evidence [SOE]). Data on NSAIDs were derived from five systematic reviews (13,214 patients; most studied was ibuprofen, followed by diclofenac and ketorolac). Compared with placebo, NSAIDs probably resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (moderate SOE). For other interventions, we included 135 RCTs and 6 comparative observational studies (37,653 patients). Compared with placebo, antiemetics (low SOE), dihydroergotamine (moderate to high SOE), ergotamine plus caffeine (moderate SOE), and acetaminophen (moderate SOE) reduced acute pain. Opioids were evaluated in 15 studies (2,208 patients).Butorphanol, meperidine, morphine, hydromorphone, and tramadol in combination with acetaminophen may reduce pain at 2 hours and 1 day, compared with placebo (low SOE). Some opioids may be less effective than some antiemetics or dexamethasone (low SOE). No studies evaluated instruments for predicting risk of opioid misuse, opioid use disorder, or overdose, or evaluated risk mitigation strategies to be used when prescribing opioids for the acute treatment of episodic migraine. Calcitonin gene-related peptide (CGRP) receptor antagonists improved headache relief at 2 hours and increased the likelihood of being headache-free at 2 hours, at 1 day, and at 1 week (low to high SOE). Lasmiditan (the first approved 5-HT1F receptor agonist) restored function at 2 hours and resolved pain at 2 hours, 1 day, and 1 week (moderate to high SOE). Sparse and low SOE suggested possible effectiveness of dexamethasone, dipyrone, magnesium sulfate, and octreotide. Compared with placebo, several nonpharmacologic treatments may improve various measures of pain, including remote electrical neuromodulation (moderate SOE), magnetic stimulation (low SOE), acupuncture (low SOE), chamomile oil (low SOE), external trigeminal nerve stimulation (low SOE), and eye movement desensitization re-processing (low SOE). However, these interventions, including the noninvasive neuromodulation devices, have been evaluated only by single or very few trials. Conclusions. A number of acute treatments for episodic migraine exist with varying degrees of evidence for effectiveness and harms. Use of triptans, NSAIDs, antiemetics, dihydroergotamine, CGRP antagonists, and lasmiditan is associated with improved pain and function. The evidence base for many other interventions for acute treatment, including opioids, remains limited.