No description available.

O mecanismo pelo qual a sinalização da leptina no hipotálamo permite o início da puberdade ainda não foi esclarecido. Um possível mecanismo para a ação molecular da leptina no eixo reprodutivo é constituído por uma alteração na sinalização do NPY. Objetivou-se neste estudo foi verificar se novilhas precoces Bos taurus indicus possuem a expressão modificada de genes hipotalâmicos relacionadas à sinalização da leptina. Dentre uma população de 500 novilhas entre 20 e 25 meses de idade, 100 novilhas foram selecionadas com base nas características da raça (Nelore), mês de nascimento e peso corpóreo (290 kg). Estas 100 novilhas foram classificadas de acordo com a presença ou não de um corpo lúteo (CL) notável. Dez novilhas sem um CL e dez novilhas com CL notável receberam uma injeção de prostaglandina, e de acordo com a observação visual de cio e palpação retal, 6 novilhas precoces e 6 novilhas não precoces foram selecionadas para o experimento. Estas 12 novilhas foram abatidas e amostras de tecido do hipotálamo foram coletadas e congeladas em nitrogênio liquido. A expressão de SOCS-3, NPY, NPY-Y1 e NPY-Y4 no hipotálamo foi quantificada por PCR em tempo real usando uma proteína ribossomal RP-L19 como um gene de referência. A expressão hipotalâmica de SOCS-3 ou NPY não foi diferente entre os grupos de novilhas (P > 0,50). Acreditava-se que as novilhas ciclando poderiam ser resistentes à leptina devido a um aumento na expressão do SOCS-3 no hipotálamo. Houve uma tendência (P = 0,10) de redução na expressão dos receptores do NPY, NPY-Y1 e NPY-Y4 em novilhas que atingiram a puberdade precocemente. A expressão do NPY-Y1 foi 8.3 vezes menor e a expressão do NPY-Y4 foi 14.3 vezes menor em novilhas precoces. Quando analisados em conjunto, houve uma redução de 11 vezes na expressão dos receptores de NPY em novilhas precoces, e este efeito foi estatisticamente significante (P = 0,03). Estes resultados sugerem que, a menor expressão dos receptores de NPY pelo hipotálamo de novilhas precoces pode torná-lo menos sensível à inibição do NPY, e permitir a obtenção da puberdade com maior peso vivo e níveis menores de leptina circulante. Em conclusão, não houve uma correlação entre a expressão do gene NPY e SOCS-3 e a precocidade sexual das novilhas Nelore, porém houve uma tendência significativa de redução da expressão dos receptores de NPY-Y1 e NPY-Y4 no hipotálamo das novilhas precoces. / The molecular mechanism by which leptin signaling in the hypothalamus might permit the initiation of puberty has not been elucidated. One possible mechanism for leptin molecular action on the reproductive axis is affecting NPY signaling. It was our objective to test whether early-maturing Bos indicus heifers have altered expression of hypothalamic genes related to leptin signaling. Among a population of 500 heifers between 20 and 25 months of age, 100 heifers were selected base on breed attributes (Nelore), month of birth, and body weight (290 kg). These 100 heifers were scored as prepubertal or pubertal according to the presence or not of a noticeable corpus luteum (CL). Ten heifers without a CL and ten heifers with noticeable CL received a prostaglandin injection, and according to visual observation of heat and rectal palpation, 6 prepubertal and 6 pubertal heifers were selected for the experiment. These 12 heifers were slaughtered and samples of hypothalamus were collected and frozen in liquid nitrogen. Expression of SOCS-3, NPY, NPY-Y1 and NPY-Y4 at the hypothalamus was quantified by real-time PCR using the ribosomal protein RP-L19 as a reference gene. Hypothalamic expression of SOCS-3 or NPY was not different between groups of heifers (P > 0, 50). It was thought that late-maturing heifers could be resistant to leptin due to an increased expression of SOCS-3 at the hypothalamus. However, there was a tendency for NPY-Y1 and NPY-Y4 expression to be reduced in heifers that reached puberty earlier (P = 0,10). Expression of NPY-Y1 was 8.3-folds lower and NPY-Y4 expression was 14.3-folds lower in early-maturing heifers. When analyzed together, there was an 11-fold reduction in NPY receptors expression in early-maturing heifers, and this effect was statistically significant (P = 0,03). These results suggest that, because of the lower expression of NPY receptors, the hypothalamus of early-maturing heifers could be less sensitive to NPY inhibition, and therefore reach puberty with lower levels of circulating leptin. In conclusion, there was no effect between the expression of NPY and SOCS-3 and sexual precocity of Nelore heifers, but there was a significant tendency of reduction in NPY-Y1 e NPY-Y4 receptors expression in the hypothalamus of sexually precocious heifers.

O mecanismo pelo qual a sinalização da leptina no hipotálamo permite o início da puberdade ainda não foi esclarecido. Um possível mecanismo para a ação molecular da leptina no eixo reprodutivo é constituído por uma alteração na sinalização do NPY. Objetivou-se neste estudo foi verificar se novilhas precoces Bos taurus indicus possuem a expressão modificada de genes hipotalâmicos relacionadas à sinalização da leptina. Dentre uma população de 500 novilhas entre 20 e 25 meses de idade, 100 novilhas foram selecionadas com base nas características da raça (Nelore), mês de nascimento e peso corpóreo (290 kg). Estas 100 novilhas foram classificadas de acordo com a presença ou não de um corpo lúteo (CL) notável. Dez novilhas sem um CL e dez novilhas com CL notável receberam uma injeção de prostaglandina, e de acordo com a observação visual de cio e palpação retal, 6 novilhas precoces e 6 novilhas não precoces foram selecionadas para o experimento. Estas 12 novilhas foram abatidas e amostras de tecido do hipotálamo foram coletadas e congeladas em nitrogênio liquido. A expressão de SOCS-3, NPY, NPY-Y1 e NPY-Y4 no hipotálamo foi quantificada por PCR em tempo real usando uma proteína ribossomal RP-L19 como um gene de referência. A expressão hipotalâmica de SOCS-3 ou NPY não foi diferente entre os grupos de novilhas (P > 0,50). Acreditava-se que as novilhas ciclando poderiam ser resistentes à leptina devido a um aumento na expressão do SOCS-3 no hipotálamo. Houve uma tendência (P = 0,10) de redução na expressão dos receptores do NPY, NPY-Y1 e NPY-Y4 em novilhas que atingiram a puberdade precocemente. A expressão do NPY-Y1 foi 8.3 vezes menor e a expressão do NPY-Y4 foi 14.3 vezes menor em novilhas precoces. Quando analisados em conjunto, houve uma redução de 11 vezes na expressão dos receptores de NPY em novilhas precoces, e este efeito foi estatisticamente significante (P = 0,03). Estes resultados sugerem que, a menor expressão dos receptores de NPY pelo hipotálamo de novilhas precoces pode torná-lo menos sensível à inibição do NPY, e permitir a obtenção da puberdade com maior peso vivo e níveis menores de leptina circulante. Em conclusão, não houve uma correlação entre a expressão do gene NPY e SOCS-3 e a precocidade sexual das novilhas Nelore, porém houve uma tendência significativa de redução da expressão dos receptores de NPY-Y1 e NPY-Y4 no hipotálamo das novilhas precoces. / The molecular mechanism by which leptin signaling in the hypothalamus might permit the initiation of puberty has not been elucidated. One possible mechanism for leptin molecular action on the reproductive axis is affecting NPY signaling. It was our objective to test whether early-maturing Bos indicus heifers have altered expression of hypothalamic genes related to leptin signaling. Among a population of 500 heifers between 20 and 25 months of age, 100 heifers were selected base on breed attributes (Nelore), month of birth, and body weight (290 kg). These 100 heifers were scored as prepubertal or pubertal according to the presence or not of a noticeable corpus luteum (CL). Ten heifers without a CL and ten heifers with noticeable CL received a prostaglandin injection, and according to visual observation of heat and rectal palpation, 6 prepubertal and 6 pubertal heifers were selected for the experiment. These 12 heifers were slaughtered and samples of hypothalamus were collected and frozen in liquid nitrogen. Expression of SOCS-3, NPY, NPY-Y1 and NPY-Y4 at the hypothalamus was quantified by real-time PCR using the ribosomal protein RP-L19 as a reference gene. Hypothalamic expression of SOCS-3 or NPY was not different between groups of heifers (P > 0, 50). It was thought that late-maturing heifers could be resistant to leptin due to an increased expression of SOCS-3 at the hypothalamus. However, there was a tendency for NPY-Y1 and NPY-Y4 expression to be reduced in heifers that reached puberty earlier (P = 0,10). Expression of NPY-Y1 was 8.3-folds lower and NPY-Y4 expression was 14.3-folds lower in early-maturing heifers. When analyzed together, there was an 11-fold reduction in NPY receptors expression in early-maturing heifers, and this effect was statistically significant (P = 0,03). These results suggest that, because of the lower expression of NPY receptors, the hypothalamus of early-maturing heifers could be less sensitive to NPY inhibition, and therefore reach puberty with lower levels of circulating leptin. In conclusion, there was no effect between the expression of NPY and SOCS-3 and sexual precocity of Nelore heifers, but there was a significant tendency of reduction in NPY-Y1 e NPY-Y4 receptors expression in the hypothalamus of sexually precocious heifers.

Diabetes mellitus (DM) is the 4th leading cause of mortality in Taiwan. Chronic persistent inflammation as demonstrated by higher proinflammatory mediators in blood has been correlated to cardiovascular complications of type 2 DM. The cellular and molecular mechanism of chronic inflammation in type 2 DM remains to be determined. This study was conducted to explore altered innate immunity in toll-like receptor (TLR) expression and signaling of monocytes from type 2 DM patients. Blood leukocytes from type 2 DM patients were counted and studied for TLR2 and TLR4 expression and signaling. Each experiment was run with 1 to 2 type 2 DM patients, simultaneously with 1 to 2 age-matched normal adults as controls. 31 type 2 DM patients and 37 normal age-matched controls completed the study. Results showed that blood monocytes from type 2 DM patients had a significantly higher TLR4 but not TLR2 expression. Using a TLR4 ligand, lipopolysaccharide (LPS), to trigger TNF£\ production, a significantly higher TNF£\ production by blood leukocytes from type 2 DM patients than age-matched controls was found. The higher TNF£\ production by blood leukocytes from type 2 DM patients was associated with down-regulation of suppressor of cytokine signaling 1and 3 (SOCS-1 and SOCS-3) expression. We have further postulated that increase of oxidative stress or decrease of IFN-£\ production in type 2 DM patients was related to the alteration of TLR-4 response. Correction of SOCS-1 expression by addition of antioxidant, superoxide dismutase (SOD), but not IFN-£\, significantly decreased TNF£\ production in blood leukocytes from type 2 DM patients. This study is the first in the literature to identify an alteration of TLR4 expression associated with depressed SOCS-1 expression in leukocytes of type 2 DM patients. Results from this study highlight a potential pathway to improve chronic inflammation of type 2 DM patients via modulation of TLR4 expression and SOCS-1 mRNA expression of leukocytes.

No description available.

Le facteur d'activation plaquettaire (PAF) est un puissant médiateur pro-inflammatoire impliqué dans des processus physiologiques et pathologiques.Le PAF exerce ses effets suite à la liaison à son récepteur, le récepteur du PAF (PAFR), qui est un récepteur à sept domaines transmembranaires et couplé aux protéines G (RCPG). La signalisation du PAFR est en partie médiée par les protéines G et implique principalement des sous-unités G[indice inférieur [alpha]i] et G[indice inférieur [alpha]q] dans plusieurs types cellulaires.Le PAFR peut également activer des effecteurs variés : des canaux ioniques, des phospholipases (PLA[indice inférieur 2], PLC, PLD), ainsi que plusieurs kinases (PKC, PI3K et MAPK). Nous avons récemment démontré que le PAFR peut activer de façon indépendante des protéines G la voie des Janus kinase (JAK) et des Signal Transducers and Activators of Transcription (STAT). JAK2, TYK2 et STAT1, 2, 3 et 5 sont ainsi activés dans la lignée cellulaire myéloïde humaine MonoMac1. Les SOCS sont une famille de protéines qui régulent négativement la signalisation des cytokines et qui ont récemment été démontrés comme impliqués dans la signalisation de certains RCPG dont le CXCR4 (récepteur de chimiokine 4 de la famille des C-X-C) et l'AT1 (récepteur de l'angiotensine II). Une stimulation au PAF induit de manière transcriptionnelle l'accumulation de l'ARNm de la protéine suppressors of cytokine signalling 3 (SOCS3) dans les monocytes humains et la lignée cellulaire MonoMac1, mais ne l'induit pas dans les cellules endothéliales de veines de cordons ombilicaux humain (HUVEC). En plus d'une augmentation de l'ARNm de SOCS3, une augmentation de la protéine SOCS3 est également observée suivant une stimulation au PAF. Premièrement, nous voulions déterminer l'importance de SOCS3 dans la signalisation du PAFR à l'aide de différentes lignées cellulaires (HEK293, COS7, MonoMac1) et diverses techniques de biologie cellulaire. Ensuite, nous désirions évaluer l'impact des différents domaines de SOCS3 dans ces fonctions par des approches de biologie moléculaire. Finalement, nous avons évalué le/s rôle/s de SOCS3 sur différents aspects fonctionnels pro-inflammatoires du PAF (Voies signalisation, adhésion cellulaires, etc.). Nous démontrons dans la présente thèse que SOCS3 module la signalisation du PAFR en plus de présenter certains aspects moléculaires entourant la relation entre le PAFR, TYK2 et SOCS3. Les présents travaux démontrent que SOCS3 peut être recruté de façon transitoire à la seconde boucle intracellulaire et la queue cytoplasmique du PAFR. Son domaine kinase inhibitory region (KIR) semble être requis pour le recrutement induit au PAFR, alors que son domaine SOCS box semble être impliqué dans le recrutement basal. Suivant une stimulation au PAF, SOCS3 est phosphorylé sur un/des résidus tyrosine. Cette modification est sous le contrôle essentiel de TYK2, alors que son mutant K930I (kinase inactive) ne le fait pas. SOCS3 joue un rôle très important dans la modulation des voies de signalisation du PAFR ainsi que sur certains effets biologiques de celui-ci. Ces actions se révèlent être également très spécifiques : SOCS3 ne module pas la voie de G[indice inférieur [alpha]q] (IP3 ), mais module la migration et également l'adhésion cellulaire induite par le PAF. SOCS3 ne module pas la phosphorylation des STAT 1, 3 et 5 induite par le PAF, mais module négativement la voie de TYK2 (activation du promoteur du PAFR) et la phosphorylation des STAT 1, 3 et 5 induite par l'OSM. SOCS3 ne module pas la voie des JNK MAPK, prolonge la voie des ERK MAPK et module négativement l'activation précoce de la voie de p38 MAPK. Enfin, SOCS3 joue un rôle de modulation négative dans la transcription induite par le PAF des promoteurs du PAFR, de l'IL-6 et de l'IL-8. En conclusion, cette thèse propose de nouveaux mécanismes par lesquels SOCS3 module certains aspects de la signalisation et effets biologiques du PAF et de son PAFR. Comme le PAF est impliqué dans plusieurs phénomènes à caractères inflammatoires, le travail présenté ici a porté son attention sur plusieurs aspects pro-inflammatoires du PAF plutôt que sur une pathologie en particulier, ce qui permettra de mieux comprendre divers aspects liant le PAFR, la kinase TYK2 et SOCS3.

Behçet’s disease (BD) is a chronic, multi systemic, recurrent vasculitis disease of unknown aetiology. The clinical manifestations are composed of relapsing episodes of recurrent oral ulcers, uveitis, skin lesions and genital ulcers along with musculoskeletal and neurological involvement. Pro-inflammatory cytokines are a key feature of the disease but the triggers for their induction are not well understood and/or controversial. Many cytokines (including IFNγ, IL-12, IL-23, IL-10 and IL-6) activate the JAK-STAT signalling pathway which is negatively regulated by Suppressor of Cytokine Signalling (SOCS) proteins. Therefore, it was hypothesised that SOCS proteins may be dysregulated in BD. The expression of SOCS 1-3 mRNA and protein was studied in peripheral blood mononuclear cells (PBMCs), Neutrophils and buccal mucosal cells (BMC) of BD patients and compared with healthy controls (HC) and recurrent aphthous stomatitis (RAS) patients. SOCS 1 and 3 were significantly upregulated in PBMCs of BD patients compared with HC (p=0.0149; p=0.0007) and there were subtle differences between expression in relapsed and symptom free BD (quiet BD). SOCS1 and SOCS 3 also significantly upregulated in BMC from oral ulcers of BD compared with HC (both at p=0.0001). Cytokines were examined in serum, saliva and culture supernatants from stimulated PBMCs. IL-6 were significantly upregulated in the saliva of relapsed BD patients compared with HC (p=0.0104) and the capacity for IL-10 secretion from BD was compromised. Phosphorylation of STATs, transcription factors RORγt, T-bet and 48 protein kinases were investigated using a novel PhosphFlow method and by microarray analysis. STATs were upregulated in BD and seven novel kinase proteins showed differential phosphorylation in BD. Conclusion: SOCS 1-3 expression has changed in BD patients with differences in PBMC and Neutrophil expression between the SOCS proteins. Phosphorylation of STATs and several kinases show up-regulation in BD and seven kinases with altered phosphorylation states in BD were identified as novel targets for future investigation.

The primary adaptive organismal response to stress involves the activation of the hypothalamic-sympathetic-chromaffin cell (HSC) axis leading to rapid secretion of catecholamines, predominantly epinephrine. The hypothalamus-pituitary-interrenal (HPI) axis activation follows, leading to the secretion of cortisol in teleosts. Both these hormones play key roles in fueling the increased energy demand associated with stress. On prolonged exposure to periods of chronic stress, the stress response shifts from adaptive to maladaptive, eventually resulting in decreased disease resistance, reduced growth and an overall decline in fitness. This reduction of performance can be viewed as a consequence of the animals altered energy budget, with an increase in the metabolic requirements to cope with stress, leading to a reduction in body defense and growth potential. However, the mechanisms linking stress effects on growth and immune performance are far from clear. The suppressors of cytokine signalling (SOCS) are gaining increasing attention in mammalian models and particularly in human medicine for their ability to regulate diverse physiological functions like immunity, growth and development. Even though homologues of the SOCS genes have been identified in fishes, their functional roles are unknown. This paucity of information on the role of SOCS, combined with the knowledge that they are key regulators of energy demanding pathways in mammals, led to the hypothesis that the SOCS genes may be playing a critical role during stress to divert energy away from immune and growth processes in fishes. To test this, liver was used as a model because this tissue plays an important role in stress adaptation, immune response and growth. The ability of cortisol to modulate immune responses in the liver was investigated by exposing rainbow trout (Oncorhynchus mykiss) hepatocytes to lipopolysaccharide (LPS), a potent immunostimulant, along with cortisol and mifepristone- a glucocorticoid receptor (GR) antagonist, to tease out the role of cortisol signalling on immune function. The results showed that LPS stimulation increases the cellular stress response and metabolic capacity and induces the expression of innate response mediators in trout hepatocytes. Cortisol modulates these responses and this involves GR signalling. The results demonstrated for the first time that cortisol upregulates SOCS-1 and SOCS-2 mRNA abundance in trout liver, leading to the proposal that these proteins may be involved in stress/cortisol-mediated immune suppression. The SOCS are also potentially involved in energy–reallocations associated with nutritional restriction. To test this, immune responses and SOCS regulation in response to LPS challenge were investigated between two salmonids exhibiting different life-strategies, the anadromous Arctic charr (Salvelinus alpinus), which undergo natural long-term fasting, and the rainbow trout, that do not naturally fast. Arctic charr and rainbow trout were fed or fasted for 85 and 118 d, respectively, and injected with LPS to examine their ability to evoke an immune response despite their negative energy balance. While fasting did not alter stress parameters like plasma cortisol and glucose levels in the Arctic charr, nutrient restriction modified plasma glucose and lactate levels and liver glycogen content in rainbow trout. Additionally the fasted charr showed lower cytokine responses to LPS than the fed charr, while there was no difference in the degree of cytokine responses between the fed and fasted rainbow trout. Fasting also upregulated SOCS isoforms in the Arctic charr, but reduced SOCS-1 expression in rainbow trout. LPS upregulated SOCS-3 in the Arctic charr, but downregulated SOCS-2 levels in rainbow trout. Together, these results suggest differences in the stress, cytokine and SOCS responses to fasting and LPS stimulation between these two salmonid species. Specifically, SOCS upregulation by fasting in charr may be adaptive to restrict energy demanding pathways, including inflammatory response and growth, to cope with the negative energy balance during overwintering. To assess if SOCS are acutely regulated by stress and if this response was modulated by fasting and LPS stimulation, trout were fed or fasted for 118 d and then injected with LPS, and 72 h later subjected to a handling disturbance. Prior fasting and LPS stimulation altered the acute stressor-mediated changes in plasma cortisol, glucose and lactate levels and liver glycogen content and GR expression in trout. Acute stress also modulated liver SOCS-2 and SOCS-3 mRNA levels in rainbow trout. Overall the results suggest that liver SOCS-2 upregulation by acute stress may be playing a role in the metabolic adjustments essential to cope with stress in fishes. Finally, a series of in vitro studies to identify possible mechanisms involved in SOCS mediated immune and growth suppression were carried out. The objective was to examine whether upregulation of SOCS genes, a key negative regulator of JAK/STAT signalling by cortisol, is a key molecular link in the suppression of growth and immune responses during stress in fish. Cortisol exposure suppressed growth hormone (GH)-stimulated insulin like growth factor (IGF-1) expression and this involved reduced STAT5 phosphorylation/ activation and decreased total JAK2 protein levels. Cortisol also suppressed LPS-induced IL-6 transcript levels. While LPS reduced GH signalling, this was mediated by the downregulation of GH receptors and not due to upregulation of SOCS genes. These results highlight a novel molecular mechanism, involving SOCS upregulation by cortisol, linking stress effects on growth and immune suppression in rainbow trout. Altogether, the results for the first time highlight novel functional roles for the SOCS genes as regulators and integrators of stress-immune-growth processes, and the mode of action involves their regulation by cortisol signalling in fishes.

The islets of Langerhans secrets insulin in response to fluctuations of blood glucose level and efficient secretion requires extensive intra-islet communication. Secretory failure from islets is one of the hallmark in progression of type 2 diabetes.  Changes in islet structure and high levels of saturated free fatty acids may contribute to this failure. The aim of this thesis is to study the role of cell-cell interactions and palmitate on β-cells functions. To address the role of cell-cell interactions on β-cells functions MIN6 cells were cultured as monolayers and as pseudoislets. Glucose stimulated insulin secretion was higher in pseudoislets compared to monolayers. Transcript levels of mitochondrial metabolism as well glucose oxidation rate was higher in pseudoislets. Insulin receptor substrate-1 (IRS-1) phosphorylation was altered when cells were grown as pseudoislets. Proteins expression levels related to glycolysis, cellular connections and translational regulations were up-regulated in pseudoislets. We propose the superior capacity of pseudoislets compared to monolayers depend on metabolism, cell coupling, gene translation, protein turnover and differential IRS-1 phosphorylation. To address the role of palmitate on β-cells human islets were cultured in palmitate. Long term palmitate treatment decreased insulin secretion which is associated with up-regulation of suppressor of cytokine signaling-2 (SOCS2) and protein inhibitor of activated STAT-1 (PIAS1). Up-regulation of SOCS2 decreased phosphorylation of Akt at site T308, whereas PIAS1 decreased protein level of ATP- citrate lyase (ACLY) and ATP synthase subunit B (ATP5B). We propose long term palmitate treatment reduces phosphatidylinositol 3-kinase (PI3K) activity, attenuates formation of acetyl-CoA and decreases ATP synthesis which may aggravate β-cells dysfunction.

Made available in DSpace on 2014-06-12T15:59:36Z (GMT). No. of bitstreams: 2 arquivo5342_1.pdf: 1635663 bytes, checksum: 8b17150a09a68bf3edb4a462d481c800 (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2006 / A capacidade de reconfiguração tem se tornado uma característica de grande importância em projetos de sistema digitais completos em um único circuito integrado (System-on-Chips). A demanda por sistemas cada vez mais flexíveis e com grande poder computacional vem demonstrar o crescente interesse por esta área de pesquisa. Neste contexto, a computação reconfigurável vem oferecer um compromisso entre as vantagens do hardware de funcionalidade fixa, e a flexibilidade dos processadores programáveis por software [ADR1.2]. Porém, existe uma certa necessidade por ferramentas e metodologias de projeto que dêem o suporte necessário à construção de SoCs reconfiguráveis [BEN05], cujas aplicações são de extrema complexidade. Neste sentido, o projeto ADRIATIC [ADR1.2] [ADR2.1] [ADR2.2] propõe o desenvolvimento de uma metodologia de projeto de hardware/software co-design e co-verificação, em alto nível, para aplicações Wireless reais, procurando atenuar esta deficiência. De forma similar, o trabalho de pesquisa proposto visa o desenvolvimento de uma metodologia de projeto, em alto nível, que possibilite a implementação de projetos de SoCs, com módulos dinamicamente reconfiguráveis, utilizando a linguagem de descrição de sistemas, SystemC [SYS03] [SYS02], com o objetivo de construir um modelo executável para o sistema projetado