Efeitos da obesidade induzida por dieta sobre a resposta vascular adaptativa ao estresse agudo em ratos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Alterações cardiovasculares e desenvolvimento de obesidade em animais submetidos à dieta hipercalórica e estresse crônico

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Envolvimento do inflamassoma e citocinas na resposta imunológica em infecção induzida pelo fungo Sporothrix schenckii

Pós-graduação em Biociências e Biotecnologia Aplicadas à Farmácia - FCFAR

Análise proteômica da resposta ao arsênio e do exoproteoma de Chromobacterium violaceum

A Chromobacterium violaceum é uma beta-proteobactéria Gram-negativa comum da microbiota tropical e um patógeno oportunista para animais e humanos. A infecção causada pela C. violaceum apresenta alta taxa de mortalidade, mas os mecanismos da patogenicidade ainda não foram caracterizados. Como outros microorganismos ambientais, essa bactéria está exposta a condições externas muito variáveis, que exigem grande adaptabilidade e sistemas de proteção eficientes. Entre esses sistemas encontra-se um operon arsRBC de resistência ao arsênio, metaloide danoso à saúde humana associado a lesões de pele, doenças neurológicas e câncer. O objetivo deste trabalho foi investigar as alterações na expressão proteica de C. violaceum ATCC 12472 na presença do arsenito e caracterizar as diversas proteínas secretadas pela bactéria. As proteínas da C. violaceum foram analisadas por eletroforese bidimensional e espectrometria de massas. A análise proteômica revelou que o arsenito induz um aumento na quantidade das proteínas envolvidas na resposta ao estresse oxidativo, reparo do DNA e metabolismo energético. Entre as proteínas secretadas, foram identificados fatores de virulência (metalopeptidases, colagenase e toxinas), transportadores, proteínas de proteção contra estresses e com potencial aplicação biotecnológica. Os resultados mostraram que a C. violaceum possui um arsenal molecular de adaptação que a torna capaz de conservar suas atividades celulares e provocar lesões em outros organismos.

Estudo dose-resposta e perfil de expressão gênica do herbicida diuron [3-(3,4-diclofenil)-1,1-dimetiluréia] em bexiga urinária de ratos wistar machos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeito imunomodulador de baixas concentrações de antineoplásicos

Pós-graduação em Patologia - FMB

Efeito do cloreto de cádmio sobre as gônadas de girinos de rãs-touro (Lithobates catesbeianus)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Death-associated odors induce stress in zebrafish

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Decreased rate of protein synthesis, caspase-3 activity, and ubiquitin-proteasome proteolysis in soleus muscles from growing rats fed a low-protein, high-carbohydrate diet

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Effects of exercise training on stress-induced vascular reactivity alterations: role of nitric oxide and prostanoids

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Alterations of protein expression in conditions of copper-deprivation for Paracoccidioides lutzii in the presence of extracellular matrix components

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Anatomia de espécies brasileiras de Eriocaulaceae: Comanthera e Syngonanthus

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

A possible increase of activity of endothelial l-arginine/nitric oxide pathway in aortas of diet-induced obesity rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Sexual Risk Recognition Deficits: The Role of Prior Victimization and Emotion Dysregulation

Recent theoretical writings suggest that the ineffective regulation of negative emotional states may reduce the ability of women to detect and respond effectively to situational and interpersonal factors that increase risk for sexual assault. However, little empirical research has explored this hypothesis. In the present study, it was hypothesized that prior sexual victimization and negative mood state would each independently predict poor risk recognition and less effective defensive actions in response to an analogue sexual assault vignette. Further, these variables were expected to interact to produce particularly impaired risk responses. Finally, that the in vivo emotion regulation strategy of suppression and corresponding cognitive resource usage (operationalized as memory impairment for the vignette) were hypothesized to mediate these associations. Participants were 668 female undergraduate students who were randomly assigned to receive a negative or neutral film mood induction followed by an audiotaped dating interaction during which they were instructed to indicate when the man had “gone too far” and describe an adaptive response to the situation. Approximately 33.5% of the sample reported a single victimization and 10% reported revictimization. Hypotheses were largely unsupported as sexual victimization history, mood condition, and their interaction did not impact risk recognition or adaptive responding. However, in vivo emotional suppression and cognitive resource usage were shown to predict delayed risk recognition only. Findings suggest that contrary to hypotheses, negative mood (as induced here) may not relate to risk recognition and response impairments. However, it may be important for victimization prevention programs that focus on risk perception to address possible underlying issues with emotional suppression and limited cognitive resources to improve risk perception abilities. Limitations and future directions are discussed.

Focal adhesion kinase governs cardiac concentric hypertrophic growth by activating the AKT and mTOR pathways

The heart responds to sustained overload by hypertrophic growth in which the myocytes distinctly thicken or elongate on increases in systolic or diastolic stress. Though potentially adaptive, hypertrophy itself may predispose to cardiac dysfunction in pathological settings. The mechanisms underlying the diverse morphology and outcomes of hypertrophy are uncertain. Here we used a focal adhesion kinase (FAK) cardiac-specific transgenic mice model (FAK-Tg) to explore the function of this non-receptor tyrosine kinase on the regulation of myocyte growth. FAK-Tg mice displayed a phenocopy of concentric cardiac hypertrophy, reflecting the relative thickening of the individual myocytes. Moreover, FAK-Tg mice showed structural, functional and molecular features of a compensated hypertrophic growth, and preserved responses to chronic pressure overload. Mechanistically, FAK overexpression resulted in enhanced myocardial FAK activity, which was proven by treatment with a selective FAK inhibitor to be required for the cardiac hypertrophy in this model. Our results indicate that upregulation of FAK does not affect the activity of Src/ERK1/2 pathway, but stimulated signaling by a cascade that encompasses PI3K, AKT, mTOR, S6K and rpS6. Moreover, inhibition of the mTOR complex by rapamycin extinguished the cardiac hypertrophy of the transgenic FAK mice. These findings uncover a unique role for FAK in regulating the signaling mechanisms that governs the selective myocyte growth in width, likely controlling the activity of PI3K/AKT/mTOR pathway, and suggest that FAK activation could be important for the adaptive response to increases in cardiac afterload. This article is part of a Special Issue entitled "Local Signaling in Myocytes". (C) 2011 Elsevier Ltd. All rights reserved.