901 resultados para sensorisk deprivation.
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Protein deficiency is one of the biggest public health problems in the world, accounting for about 30-40% of hospital admissions in developing countries. Nutritional deficiencies lead to alterations in the peripheral nervous system and in the digestive system. Most studies have focused on the effects of protein-deficient diets on the enteric neurons, but not on sympathetic ganglia, which supply extrinsic sympathetic input to the digestive system. Hence, in this study, we investigated whether a protein-restricted diet would affect the quantitative structure of rat coeliac ganglion neurons. Five male Wistar rats (undernourished group) were given a pre- and postnatal hypoproteinic diet receiving 5% casein, whereas the nourished group (n = 5) was fed with 20% casein (normoproteinic diet). Blood tests were carried out on the animals, e.g., glucose, leptin, and triglyceride plasma concentrations. The main structural findings in this study were that a protein-deficient diet (5% casein) caused coeliac ganglion (78%) and coeliac ganglion neurons (24%) to atrophy and led to neuron loss (63%). Therefore, the fall in the total number of coeliac ganglion neurons in protein-restricted rats contrasts strongly with no neuron losses previously described for the enteric neurons of animals subjected to similar protein-restriction diets. Discrepancies between our figures and the data for enteric neurons (using very similar protein-restriction protocols) may be attributable to the counting method used. In light of this, further systematic investigations comparing 2-D and 3-D quantitative methods are warranted to provide even more advanced data on the effects that a protein-deficient diet may exert on sympathetic neurons. (C) 2009 Wiley-Liss, Inc.
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Purpose We investigated the effects of ischemia/reperfusion in the intestine (I/R-i) on purine receptor P2X(2)-immunoreactive (IR) neurons of the rat ileum. Methods The superior mesenteric artery was occluded for 45 min with an atraumatic vascular clamp and animals were sacrificed 4 h later. Neurons of the myenteric and submucosal plexuses were evaluated for immunoreactivity against the P2X(2) receptor, nitric oxide synthase (NOS), choline acetyl transferase (ChAT), calbindin, and calretinin. Results Following I/R-i, we observed a decrease in P2X(2) receptor immunoreactivity in the cytoplasm and surface membranes of neurons of the myenteric and submucosal plexuses. These studies also revealed an absence of calbindin-positive neurons in the I/R-i group. In addition, the colocalization of the P2X(2) receptor with NOS, ChAT, and calretinin immunoreactivity in the myenteric plexus was decreased following I/R-i. Likewise, the colocalization between P2X(2) and calretinin in neurons of the submucosal plexus was also reduced. In the I/R-i group, there was a 55.8% decrease in the density of neurons immunoreactive (IR) for the P2X(2) receptor, a 26.4% reduction in NOS-IR neuron, a 25% reduction in ChAT-IR neuron, and a 47% reduction in calretinin-IR neuron. The density of P2X(2) receptor and calretinin-IR neurons also decreased in the submucosal plexus of the I/R-i group. In the myenteric plexus, P2X(2)-IR, NOS-IR, ChAT-IR and calretinin-IR neurons were reduced in size by 50%, 49.7%, 42%, and 33%, respectively, in the I/R-i group; in the submucosal plexus, P2X(2)-IR and calretinin-IR neurons were reduced in size by 56% and 72.6%, respectively. Conclusions These data demonstrate that ischemia/reperfusion of the intestine affects the expression of the P2X(2) receptor in neurons of the myenteric and submucosal plexus, as well as density and size of neurons in this population. Our findings indicate that I/R-i induces changes in P2X(2)-IR enteric neurons that could result in alterations in intestinal motility.
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Neonatal anoxia is a worldwide clinical problem that has serious and lasting consequences. The diversity of models does not allow complete reproducibility, so a standardized model is needed. In this study, we developed a rat model of neonatal anoxia that utilizes a semi-hermetic system suitable for oxygen deprivation. The validity of this model was confirmed using pulse oximetry, arterial gasometry, observation of skin color and behavior and analysis of Fos immunoreactivity in brain regions that function in respiratory control. For these experiments, 87 male albino neonate rats (Rattus norvegicus, lineage Wistar) aged approximate 30 postnatal hours were divided into anoxia and control groups. The pups were kept in an euthanasia polycarbonate chamber at 36 +/- 1 degrees C, with continuous 100% nitrogen gas flow at 3 L/min and 101.7 kPa for 25 min. The peripheral arterial oxygen saturation of the anoxia group decreased 75% from its initial value. Decreased pH and partial pressure of oxygen and increased partial pressure of carbon dioxide were observed in this group, indicating metabolic acidosis, hypoxia and hypercapnia. respectively. Analysis of neuronal activation showed Fos immunoreactivity in the solitary tract nucleus, the lateral reticular nucleus and the area postrema, confirming that those conditions activated areas related to respiratory control in the nervous system. Therefore, the proposed model of neonatal anoxia allows standardization and precise control of the anoxic condition, which should be of great value in indentifying both the mechanisms underlying neonatal anoxia and novel therapeutic strategies to combat or prevent this widespread public health problem. (C) 2011 Elsevier B.V. All rights reserved.
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Electrical coupling provided by connexins (Cx) in gap junctions (GJ) plays important roles in both the developing and the mature retina. In mammalian nocturnal species, Cx36 is an essential component in the rod pathway, the retinal circuit specialized for night, scotopic vision. Here, we report the expression of Cx36 in a species (Gallus gallus) that phylogenetic development endows with an essentially rodless retina. Cx36 gene is very highly expressed in comparison with other Cxs previously described in the adult retina, such as Cx43, Cx45, and Cx50. Moreover, real-time PCR, Western blot, and immunofluorescence all revealed that Cx36 expression massively increased over time during development. We thoroughly examined Cx36 in the inner and outer plexiform layers, where this protein was particularly abundant. Cx36 was observed mainly in the off sublamina of the inner plexiform layer rather than in the on sublamina previously described in the mammalian retina. In addition, Cx36 colocalized with specific cell markers, revealing the expression of this protein in distinct amacrine cells. To investigate further the involvement of Cx36 in visual processing, we examined its functional regulation in retinas from dark-adapted animals. Light deprivation markedly up-regulates Cx36 gene expression in the retina, resulting in an increased accumulation of the protein within and between cone synaptic terminals. In summary, the developmental regulation of Cx36 expression results in particular circuitry-related roles in the chick retina. Moreover, this study demonstrated that Cx36 onto- and phylogenesis in the vertebrate retina simultaneously exhibit similarities and particularities. J. Comp. Neurol. 512:651-663, 2009. (C) 2008 Wiley-Liss, Inc.
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We investigated the mechanisms responsible for increased blood pressure and sympathetic nerve activity (SNA) caused by 2-3 days dehydration (DH) both in vivo and in situ preparations. In euhydrated (EH) rats, systemic application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to remove the hypothalamus) significantly reduced thoracic (t) SNA. In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transections, failed to reduce tSNA, whereas transection at the medulla-spinal cord junction massively reduced tSNA. In DH but not EH rats, selective inhibition of the commissural nucleus tractus solitarii (cNTS) significantly reduced tSNA. Comparable data were obtained in both in situ and in vivo (anaesthetized/conscious) rats and suggest that following chronic dehydration, the control of tSNA transfers from supra-brainstem structures (e. g. hypothalamus) to the medulla oblongata, particularly the cNTS. As microarray analysis revealed up-regulation of AP1 transcription factor JunD in the dehydrated cNTS, we tested the hypothesis that AP1 transcription factor activity is responsible for dehydration-induced functional plasticity. When AP1 activity was blocked in the cNTS using a viral vector expressing a dominant negative FosB, cNTS inactivation was ineffective. However, tSNA was decreased after pre-collicular transection, a response similar to that seen in EHrats. Thus, the dehydration-induced switch in control of tSNA from hypothalamus to cNTS seems to be mediated via activation of AP1 transcription factors in the cNTS. If AP1 activity is blocked in the cNTS during dehydration, sympathetic activity control reverts back to forebrain regions. This unique reciprocating neural structure-switching plasticity between brain centres emphasizes the multiple mechanisms available for the adaptive response to dehydration.
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The relationship between sleep and epilepsy is both complex and clinically significant. Temporal lobe epilepsy (TLE) influences sleep architecture, while sleep plays an important role in facilitating and/or inhibiting possible epileptic seizures. The pilocarpine experimental model reproduces several features of human temporal lobe epilepsy and is one of the most widely used models in basic research. The aim of the present study was to characterize, behaviorally and electrophysiologically, the phases of sleep-wake cycles (SWC) in male rats with pilocarpine-induced epilepsy. Epileptic rats presented spikes in all phases of the SWC as well as atypical cortical synchronization during attentive wakefulness and paradoxical sleep. The architecture of the sleep-wake phases was altered in epileptic rats, as was the integrity of the SWC. Because our findings reproduce many relevant features observed in patients with epilepsy, this model is suitable to study sleep dysfunction in epilepsy. (C) 2009 Elsevier Inc. All rights reserved.
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Global gene expression analysis was carried out with Blastocladiella emersonii cells subjected to oxygen deprivation (hypoxia) using cDNA microarrays. In experiments of gradual hypoxia (gradual decrease in dissolved oxygen) and direct hypoxia (direct decrease in dissolved oxygen), about 650 differentially expressed genes were observed. A total of 534 genes were affected directly or indirectly by oxygen availability, as they showed recovery to normal expression levels or a tendency to recover when cells were reoxygenated. In addition to modulating many genes with no putative assigned function, B. emersonii cells respond to hypoxia by readjusting the expression levels of genes responsible for energy production and consumption. At least transcriptionally, this fungus seems to favor anaerobic metabolism through the upregulation of genes encoding glycolytic enzymes and lactate dehydrogenase and the downregulation of most genes coding for tricarboxylic acid (TCA) cycle enzymes. Furthermore, genes involved in energy-costly processes, like protein synthesis, amino acid biosynthesis, protein folding, and transport, had their expression profiles predominantly down-regulated during oxygen deprivation, indicating an energy-saving effort. Data also revealed similarities between the transcriptional profiles of cells under hypoxia and under iron(II) deprivation, suggesting that Fe(2+) ion could have a role in oxygen sensing and/or response to hypoxia in B. emersonii. Additionally, treatment of fungal cells prior to hypoxia with the antibiotic geldanamycin, which negatively affects the stability of mammalian hypoxia transcription factor HIF-1 alpha, caused a significant decrease in the levels of certain upregulated hypoxic genes.
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Syftet med studien var att undersöka vilka omvårdnadsåtgärder en sjuksköterska kan utföra för att minska smärta, samt att undersöka vad föräldrarna kan bidra med för att underlätta smärtan hos sitt barn.Metoden som använts är en systematisk litteraturstudie, där 15 artiklar granskades. Det finns många olika omvårdnadsåtgärder för att lindra smärtan hos ett barn, detta kan göras med hjälp av avledning, förberedande information, sensorisk fokusering, kyla, visualisering, andningsteknik, avslappning och emotionellt stöd. Sjuksköterskan kan även hjälpa genom att stötta föräldrarna. Föräldrarna kan hjälpa sina barn genom emotionellt stöd, massage, avledning och lägesändringar. Enligt uppsatsförfattarna finns det enkla sätt för sjuksköterskan att underlätta barns smärta, som inte kräver barnspecialistutbildning från sjuksköterskan. Sjuksköterskan kan t.ex. tala med barnet om något positivt i barnets liv och genom detta avleda barnet från smärtan. Uppsatsförfattarna tror att genom att stödja föräldrarna ges de modet att utföra åtgärder som kan lindra smärtan hos barnen.
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The shelter as a recurrent solution to homelessness During most of the 20th century shelters for the homeless has been criticized as being of too low standard and an unworthy way of living in a welfare society. During the 1960s and 1970s most shelters in Sweden were shut down and replaced with other forms of housing for the homeless. Since the late 1980s and early 1990s the issue of homelessness has returned to the political agenda as an existing social problem in Sweden. In this period we have also experienced a return of the shelters. These newly opened shelters are in many ways based on the same ideas like the old shelters described in stories of poverty and deprivation from the 19th century. In our article we raise the question how a system that has been rejected and condemned from both ethical and ideological standpoints as an unworthy way of living can be “remodernized” and considered again as a (temporary) solution to homelessness. We examine how shelters are justified in the 21st century and what functions they fill. We also discuss the fact that the shelters are almost exclusively run by (religious) voluntary organizations.
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Malnutrition is a worldwide problem affecting millions of unborn and young children during the most vulnerable stages of brain development (1). All restriction of protein during the perinatal period of life can alter the development of mammalian fetus and have marked repercussions on development of the Central Nervous System (CNS). The brain is vulnerable to protein malnutrition with altered morphologic and biochemical maturation, leading to impaired functions. The focus of this study is to investigate [U-14C]glycine metabolism in malnourished rats submitted to pre- and postnatal protein deprivation (diet: 8% protein with addition and without addition of L-methionine) on glycine metabolism of rats (normonourished group: 25% protein). It was observed that protein malnutrition alters oxidation to CO2, conversion to lipids and protein synthesis from [U-14C]glycine in cerebellum of malnourished rats without addition of L-methionine on a diet at 7 and 21 days of postnatal life. Our results also indicate that protein malnutrition causes a retardation in the normally ordered progression of brain development, and the malnourished groups have smaller cells, reduction in cell numbers and smaller cerebellar weight comparing to the control group.
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Uma das principais características do hipocampo após a isquemia é a vulnerabilidade diferencial das células da região CA1 e DG à morte celular. Os neurônios granulares do DG são resistentes, enquanto que os neurônios piramidais da região CA1 são mais sensíveis. Nosso objetivo nesse estudo foi investigar o possível envolvimento da via de sinalização celular PI3K, uma via que possui efeito proliferativo e antiapoptótico, e das proteínas de choque térmico (HSPs) no fenômeno da vulnerabilidade seletiva. Para isso foram usadas culturas organotípicas de hipocampo de ratos Wistar de 6-8 dias. As culturas foram tratadas com o inibidor da PI3K, LY294002 (LY), nas doses 10μM e 50μM. A morte celular foi quantificada pela medida da incorporação de iodeto de propídeo e da atividade das caspases 3 e 7. Alterações na fosforilação e no imunoconteúdo das proteínas foram obtidas com o uso de anticorpos específicos. Os resultados mostraram que a região do DG parece responder de forma tempo dependente e precocemente à presença da droga, sugerindo uma importância da via nessa região. Para investigar se a proteína AKT, uma cinase ativada por PI3K, estava envolvida na vulnerabilidade seletiva das células às condições de privação de oxigênio e glicose (POG), medimos a fosforilação e o imunoconteúdo dessa cinase após 60 minutos de POG seguida dos tempos de recuperação de 30 minutos, 6 horas e 24 horas. Nenhuma alteração foi observada nesses parâmetros, sugerindo que , nesse caso, a fosforilação da AKT não está envolvida na vulnerabilidade seletiva. Quando o imunoconteúdo da HSP27 e da HSP70 foi investigado após as condições de POG em ambas as áreas do hipocampo, não foi observada nenhuma alteração na HSP27 nos tempos de recuperação escolhidos. Por outro lado, observou-se aumento no imunoconteúdo da HSP70 em ambas as regiões 24 horas após a exposição às condições de POG, sendo este maior no CA1. Quando as quantidades das HSPs nas duas regiões em condições basais foram comparadas, observou-se que ambas estão em maior quantidade na região do DG. Esta diferença poderia estar relacionada com a resistência à morte celular observada no DG, uma vez que, possuindo maior quantidade HSPs, estas poderiam atuar como protetoras contra a morte. Esses resultados sugerem que a via de sinalização da PI3K pode estar envolvida na vulnerabilidade seletiva observada no hipocampo em resposta à condições de POG, e esta não envolve alterações na fosforilação da AKT. Por outro lado, HSP27 e HSP70 podem estar envolvidas no fenômeno da vulnerabilidade seletiva, protegendo o DG das lesões.
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A proposta básica de nosso estudo está na preocupação de identificar os princípios de uma modalidade de educação: o atendimento compensatório/remediativo, destinada às crianças das classes "desfavorecidas", os alunos "carentes", e a criação de um espaço necessário ao processo de educação dessas crianças, designado oficialmente de "Classes de Adaptação". Para dar conta de tal proposta, definimos como objeto de estudo o discurso pedagógico, como discurso dominante, dando relevo às formulações referentes à "carência", às questões levantadas em torno da criação das "Classes de Adaptação" e ao discernimento da função social de sua criação e utilização. A análise das formulações passa pela compreensão das categorias pertinentes: "marginalização cultural", "privação cultural", "marginalizado cultural", "cultura da pobreza". " Rede teórica" (cf. Foucault) que nos ajudou a pensar a importância do tema da "carência" (e do seu complemento, a "compensação"). A análise mostra que, a pretexto de "compensar" as "privações" (ou "carências") das crianças "desfavorecidas", pelas dificuldades de aprendizagem que apresentam na escola, essas crianças são encaminhadas às Classes de Adaptação, que visam disciplinar, ou seja, torná-los úteis e dóceis, em função do sistema de produção. O entendimento dessa perspectiva leva-nos a perceber as dificuldades que essas crianças apresentam na escola, não como "inadaptação cultural", concepção que em geral reproduz a versão da ideologia dominante, difundida pela escola, e sim como um problema político, em que a origem social tem um peso fundamental na sua identificação, enquanto "carentes".
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O presente trabalho consiste num estudo das Leis, Normas e Diretrizes propostas pelo Ministério da Educação e Cultura que, a partir de 1975 até 1980, tiveram maior divulgação e portanto - suponho - muita influência nas programações de educação pré-escolar dos diversos Estados e Territórios da Federação. De início ressalta-se a importância da educação pré-escolar por si mesma como condição necessária e não contingente para o desenvo1vimento humano, descartando-se as abordagens da privação cultural, base da educação compensatória. A seguir assa-se ao estudo propriamente dito dos documentos selecionados, buscando-se encontrar os propósitos, contradições, dos programas apresentados pelo Sistema Oficial de Ensino com o objetivo de contribuir para o alcance de alternativas mais coerentes. Como Metodologia de Trabalho procura-se estudar os documentos segundo a ordem cronológica de sua publicação de modo a que se possa visualizar numa progressão seqüencial, as ações relativas ao Programa de Educação Pré-Escolar no Brasil. Conclui-se que, no decorrer de aproximadamente um quinqüênio, a natureza do discurso sobre o tema foi mantida quase na íntegra e que as medidas relativas à pré-escola, de modo geral conservaram-se no papel e que, assim mesmo, estas medidas revestem-se dos princípios de "educação compensatória."
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O objetivo deste estudo foi avaliar a ocorrência de resposta compensatória no desempenho produtivo de juvenis de tilápia do Nilo Oreochromis niloticus, linhagem GIFT, submetidos a diferentes estratégias alimentares. Foram utilizados 135 juvenis de tilápia, distribuídos em nove tanques de polietileno de 100L cada. As estratégias testadas foram: grupo controle (alimentado todo dia), grupo alimentado por cinco dias seguidos de dois dias de restrição de alimento (5A/2R) e grupo alimentado por quatro dias seguidos de três dias de restrição de alimento (4A/3R). Foram avaliados parâmetros físico-químicos da água e de desempenho produtivo. Os resultados foram submetidos à análise de variância, e as médias foram comparadas pelo teste Tukey, a 5% de probabilidade. A qualidade de água, o fator de condição e a conversão alimentar não foram influenciados pela estratégia alimentar. O grupo alimentado com a estratégia 5A/2R apresentou peso final, ganho de peso e taxa de crescimento específico semelhantes ao grupo continuamente alimentado (7,8 e 9,2g; 6,4 e 7,8g e 2,7 e 3,0% dia-1, para peso final, ganho de peso e taxa de crescimento especifico, respectivamente). A estratégia 4A/3R apresentou os piores resultados de desempenho produtivo, e a estratégia 5A/2R pode ser usada na alimentação de juvenis de tilápia do Nilo sem prejuízo ao desempenho produtivo, possibilitando inclusive redução de até 22,5% na quantidade de alimento ofertada.