Educomunicação e suas áreas de intervenção: Novos paradigmas para o diálogo intercultural

oai:omp.abpeducom.org.br:publicationFormat/1O material aqui divulgado representa, em essência, a contribuição do VII Encontro Brasileiro de Educomunicação ao V Global MIL Week, da UNESCO, ocorrido na ECA/USP, entre 3 e 5 de novembro de 2016. Estamos diante de um conjunto de 104 papers executivos, com uma média de entre 7 e 10 páginas, cada um. Com este rico e abundante material, chegamos ao sétimo e-book publicado pela ABPEducom, em seus seis primeiros anos de existência. A especificidade desta obra é a de trazer as “Áreas de Intervenção” do campo da Educomunicação, colocando-as a serviço de uma meta essencial ao agir educomunicativo: o diálogo intercultural, trabalhado na linha do tema geral do evento internacional: Media and Information Literacy: New Paradigms for Intercultural Dialogue

Early and late acute lung injury and their association with distal organ damage in murine malaria

AbstractSevere malaria is characterised by cerebral oedema, acute lung injury (ALI) and multiple organ dysfunctions, however, the mechanisms of lung and distal organ damage need to be better clarified. Ninety-six C57BL/6 mice were injected intraperitoneally with 5×106 Plasmodium berghei ANKA-infected erythrocytes or saline. At day 1, Plasmodium berghei infected mice presented greater number of areas with alveolar collapse, neutrophil infiltration and interstitial oedema associated with lung mechanics impairment, which was more severe at day 1 than day 5. Lung tumour necrosis factor-α and chemokine (C-X-C motif) ligand 1 levels were higher at day 5 compared to day 1. Lung damage occurred in parallel with distal organ injury at day 1; nevertheless, lung inflammation and the presence of malarial pigment in distal organs were more evident at day 5. In conclusion, ALI develops prior to the onset of cerebral malaria symptoms. Later during the course of infection, the established systemic inflammatory response increases distal organ damage

Therapeutic effect of lipoxin A4 in malaria‐induced acute lung injury

Acute lung injury (ALI) models are characterized by neutrophil accumulation, tissue damage, alteration of the alveolar capillary membrane, and physiological dysfunction. Lipoxin A4 (LXA4) is an anti-inflammatory eicosanoid that was demonstrated to attenuate lipopolysaccharide-induced ALI. Experimental models of severe malaria can be associated with lung injury. However, to date, a putative effect of LXA4 on malaria (M)-induced ALI has not been addressed. In this study, we evaluated whether LXA4 exerts an effect on M-ALI. Male C57BL/6 mice were randomly assigned to the following five groups: noninfected; saline-treated Plasmodium berghei-infected; LXA4-pretreated P. berghei-infected (LXA4 administered 1 h before infection and daily, from days 0 to 5 postinfection), LXA4- and LXA4 receptor antagonist BOC-2-pretreated P. berghei-infected; and LXA4-posttreated P. berghei-infected (LXA4 administered from days 3 to 5 postinfection). By day 6, pretreatment or posttreatment with LXA4 ameliorate lung mechanic dysfunction reduced alveolar collapse, thickening and interstitial edema; impaired neutrophil accumulation in the pulmonary tissue and blood; and reduced the systemic production of CXCL1. Additionally, in vitro treatment with LXA4 prevented neutrophils from migrating toward plasma collected from P. berghei-infected mice. LXA4 also impaired neutrophil cytoskeleton remodeling by inhibiting F-actin polarization. Ex vivo analysis showed that neutrophils from pretreated and posttreated mice were unable to migrate. In conclusion, we demonstrated that LXA4 exerted therapeutic effects in malaria-induced ALI by inhibiting lung dysfunction, tissue injury, and neutrophil accumulation in lung as well as in peripheral blood. Furthermore, LXA4 impaired the migratory ability of P. berghei-infected mice neutrophils

Therapeutic effect of Lipoxin A 4

Acute lung injury (ALI) models are characterized by neutrophil accumulation, tissue damage, alteration of the alveolar capillary membrane, and physiological dysfunction. Lipoxin A4 (LXA4) is an anti-inflammatory eicosanoid that was demonstrated to attenuate lipopolysaccharide-induced ALI. Experimental models of severe malaria can be associated with lung injury. However, to date, a putative effect of LXA4 on malaria (M)-induced ALI has not been addressed. In this study, we evaluated whether LXA4 exerts an effect on M-ALI. Male C57BL/6 mice were randomly assigned to the following five groups: noninfected; saline-treated Plasmodium berghei-infected; LXA4-pretreated P. berghei-infected (LXA4 administered 1 h before infection and daily, from days 0 to 5 postinfection), LXA4- and LXA4 receptor antagonist BOC-2-pretreated P. berghei-infected; and LXA4-posttreated P. berghei-infected (LXA4 administered from days 3 to 5 postinfection). By day 6, pretreatment or posttreatment with LXA4 ameliorate lung mechanic dysfunction reduced alveolar collapse, thickening and interstitial edema; impaired neutrophil accumulation in the pulmonary tissue and blood; and reduced the systemic production of CXCL1. Additionally, in vitro treatment with LXA4 prevented neutrophils from migrating toward plasma collected from P. berghei-infected mice. LXA4 also impaired neutrophil cytoskeleton remodeling by inhibiting F-actin polarization. Ex vivo analysis showed that neutrophils from pretreated and posttreated mice were unable to migrate. In conclusion, we demonstrated that LXA4 exerted therapeutic effects in malaria-induced ALI by inhibiting lung dysfunction, tissue injury, and neutrophil accumulation in lung as well as in peripheral blood. Furthermore, LXA4 impaired the migratory ability of P. berghei-infected mice neutrophils

Lipoxin A4 attenuates endothelial dysfunction during experimental cerebral malaria

Submitted by sandra infurna ([email protected]) on 2016-01-28T13:59:32Z No. of bitstreams: 1 barbara_antunes_etal_IOC_2015.pdf: 906335 bytes, checksum: d9af0df9d57993f82f8cb5ec22e0e37e (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-01-28T14:16:34Z (GMT) No. of bitstreams: 1 barbara_antunes_etal_IOC_2015.pdf: 906335 bytes, checksum: d9af0df9d57993f82f8cb5ec22e0e37e (MD5)Made available in DSpace on 2016-01-28T14:16:34Z (GMT). No. of bitstreams: 1 barbara_antunes_etal_IOC_2015.pdf: 906335 bytes, checksum: d9af0df9d57993f82f8cb5ec22e0e37e (MD5) Previous issue date: 2015Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa em Malária. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Farmanguinhos. Laboratório de Farmacologia Aplicada. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde (CDTS). Instituto Nacional de Ciência e Tecnologia em Inovação para Doenças Negligenciadas (INCT/IDN). Rio de Janeiro, RJ, Brasil.A breakdown of the brain–blood barrier (BBB) due to endothelial dysfunction is a primary feature of cerebral malaria (CM). Lipoxins (LX) are specialized pro-resolving mediators that attenuate endothelial dysfunction in different vascular beds. It has already been shown that LXA4 prolonged Plasmodium berghei-infected mice survival by a mechanism that depends on inhibiting IL-12 production and CD8+IFN-γ+ T cells in brain tissue; however, the effects of this treatment on endothelial dysfunction induced during experimental cerebral malaria (ECM) remains to be elucidated. Herein, we investigate the role of LXA4 on endothelial dysfunction during ECM. The treatment of P. berghei-infected mice with LXA4 prevented BBB breakdown and ameliorated behavioral symptoms but did not modulate TNF-α production. In addition, microcirculation analysis showed that treatment with LXA4 significantly increased functional capillary density in brains of P. berghei-infected C57BL/6 mice. Furthermore, histological analyses of brain sections demonstrated that exogenous LXA4 reduced capillary congestion that was accompanied by reduced ICAM-1 expression in the brain tissue. In agreement, LXA4 treatment of endothelial cells stimulated by Plasmodium berghei (Pb)- or Plasmodium falciparum (Pf)-parasitized red blood cells (RBCs) inhibited ICAM-1 expression. Additionally, LXA4 treatment restored the expression of HO-1 that is reduced during ECM. As well, LXA4 treatment inhibits PbRBC and PfRBC adhesion to endothelial cells that was reversed by the use of an HO-1 inhibitor (ZnPPIX). Our results demonstrate for the first time that LXA4 ameliorates endothelial dysfunction during ECM by modulating ICAM-1 and HO-1 expression in brain tissue

Is there any benefit using low-intensity inspiratory and peripheral muscle training in heart failure? A randomized clinical trial

Inspiratory and peripheral muscle training improves muscle strength, exercise tolerance, and quality of life in patients with chronic heart failure (HF). However, studies investigating different workloads for these exercise modalities are still lacking.To examine the effects of low and moderate intensities on muscle strength, functional capacity, and quality of life.A randomized controlled trial.Thirty-five patients with stable HF (aged >18 years, NYHA II/III, LVEF <40%) were randomized to: non-exercise control group (n = 9), low-intensity training group (LIPRT, n = 13, 15% maximal inspiratory workload, and 0.5 kg of peripheral muscle workload) or moderate-intensity training group (MIPRT, n = 13, 30% maximal inspiratory workload and 50% of one maximum repetition of peripheral muscle workload). The outcomes were: respiratory and peripheral muscle strength, pulmonary function, exercise tolerance by the 6-minute walk test, symptoms based on the NYHA functional class, and quality of life using the Minnesota Living with Heart Failure Questionnaire.All groups showed similar quality-of-life improvements. Low and moderate intensities training programs improved inspiratory muscle strength, peripheral muscle strength, and walking distance. However, only moderate intensity improved expiratory muscle strength and NYHA functional class in HF patients.The low-intensity inspiratory and peripheral resistance muscle training improved inspiratory and peripheral muscle strength and walking distance, demonstrating that LIPRT is an efficient rehabilitation method for debilitated HF patients. In addition, the moderate-intensity resistance training also improved expiratory muscle strength and NYHA functional class in HF patients