A democracia fardada: imaginário político e negação do dissenso durante a transição brasileira (1979-1988)

O trabalho discute os limites impostos pelas Forças Armadas ao processo de democratização da sociedade brasileira durante o período que se inicia na revogação dos Atos Institucionais, em 1979, e se encerra com a promulgação da Constituinte de 1988. Entende-se que tais limites se relacionam com a identidade política fortemente anticomunista dos militares brasileiros. O material utilizado para esta discussão é o Orvil, um livro elaborado pelo Centro de Informações do Exército com o objetivo de refutar as denúncias de violações de direitos humanos cometidas por militares ao longo da ditadura instalada em 1964. Menciona-se, ainda, questões relacionadas à anistia concedida aos autores daquelas violações

El anticomunismo de la juventud conservadora chilena. el caso de la Falange Nacional (1935-1957)

This article examines anticommunist formulations in the “agendas” through which Brazilian military commanders conduct annual celebrations of two victories by the armed forces: in 1935, against the so-called “Intentona Comunista” (Communist Conspiracy); and in 1964, in the coup that overthrew the constitutional government of João Goulart. In these discourses, we seek elements that allow a characterization of military anticommunism as a political culture that guided the behavior of military institutions in Brazil throughout the twentieth century

Análise de receptores de quimiocinas na superfície de leucócitos circulantes de indivíduos infectados pelo Mycobacterium leprae: resultados preliminares

Neste estudo, a expressão de receptores de quimiocinas na superfície dos leucócitos circulantes foi feita pela citometria de fluxo. Houve aumento da porcentagem de linfócitos CCR2+CD4+ no sangue periférico dos pacientes com hanseníase. Este resultado preliminar sugeriu alteração do perfil dos receptores de quimiocinas desses pacientes

Expression of the chemokine receptor CXCR4 on lymphocytes of leprosy patients

Submitted by Nuzia Santos ([email protected]) on 2014-11-25T16:42:19Z No. of bitstreams: 1 Expression of the chemokine receptor CXCR4 on lymphocytes of leprosy patients..pdf: 219393 bytes, checksum: fd257a2469de7fd6e36b9c20f1501b9b (MD5)Approved for entry into archive by Nuzia Santos ([email protected]) on 2014-11-25T16:46:08Z (GMT) No. of bitstreams: 1 Expression of the chemokine receptor CXCR4 on lymphocytes of leprosy patients..pdf: 219393 bytes, checksum: fd257a2469de7fd6e36b9c20f1501b9b (MD5)Made available in DSpace on 2014-11-25T16:46:08Z (GMT). No. of bitstreams: 1 Expression of the chemokine receptor CXCR4 on lymphocytes of leprosy patients..pdf: 219393 bytes, checksum: fd257a2469de7fd6e36b9c20f1501b9b (MD5) Previous issue date: 2011Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brasil/Universidade Federal dos Vales do Jequitinhonha e Mucuri. Laboratório de Imunologia. Diamantina, MG, BrasilUniversidade Federal dos Vales do Jequitinhonha e Mucuri. Laboratório de Imunologia. Diamantina, MG, BrasilUniversidade Federal de Minas Gerais. Faculdade de Medicina. Departamento de Clínica Médica. Belo Horizonte, MG, BrasilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Laboratório de Imunofarmacologia. Belo Horizonte, MG, BrasilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Laboratório de Imunofarmacologia. Belo Horizonte, MG, BrasilFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Belo Horizonte, MG, BrasilFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Belo Horizonte, MG, BrasilFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Belo Horizonte, MG, Brasil/ Centro Universitário Newton Paiva. Belo Horizonte, MG, Brasil/Universidade Vale do Rio Verde. Belo Horizonte, MG, BrasilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Laboratório de Imunofarmacologia. Belo Horizonte, MG, BrasilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brasil/Universidade Federal de Minas Gerais. Faculdade de Medicina. Departamento de Clínica Médica. Belo Horizonte, MG, BrasilLeprosy is caused by Mycobacterium leprae, which induces chronic granulomatous infection of the skin and peripheral nerves. The disease ranges from the tuberculoid to the lepromatous forms, depending on the cellular immune response of the host.Chemokines are thought to be involved in the immunopathogenesis of leprosy, but few studies have investigated the expression of chemokine receptors on leukocytes of leprosy patients. In the present study, we evaluated 21 leprosy patients (M/F: 16/5) with a new diagnosis from the Dermatology Outpatient Clinic of the University Hospital, Federal University of Minas Gerais. The control group was composed of 20 healthy members (M/F: 15/5) of the community recruited by means of announcements. The expression of CCR2, CCR3, CCR5, and CXCR4 was investigated by flow cytometry on the surface of peripheral blood lymphocytes. There was a decrease in percentage of CD3+CXCR4+ and CD4+CXCR4+ lymphocytes in the peripheral blood of leprosy patients (median [range], 17.6 [2.7-41.9] and 65.3 [3.9-91.9], respectively) compared to the control group (median [range], 43.0 [3.7-61.3] and 77.2 [43.6-93.5], respectively). The percentage of CD4+CXCR4+ was significantly lower in patients with the tuberculoid form (median [range], 45.7 [0.0-83.1]) of the disease, but not in lepromatous patients (median [range], 81.5 [44.9-91.9]). The CXCR4 chemokine receptor may play a role in leprosy immunopathogenesis, probably directing cell migration to tissue lesions in tuberculoid leprosy patients

Paradoxical role of matrix metalloproteinases in liver injury and regeneration after sterile acute hepatic failure

Acetaminophen (APAP) poisoning is one of the leading causes of acute hepatic failure and liver transplantation is often the only lifesaving alternative. During the course of hepatocyte necrosis, an intense accumulation of neutrophils is often observed within the liver microenvironment. Despite the classic idea that neutrophil accumulation in tissues causes collateral tissue damage, there is a growing body of evidence showing that neutrophils can also orchestrate the resolution of inflammation. In this work, drug-induced liver injury was induced by oral administration of APAP and pharmacological intervention was made 12 h after this challenge. Liver injury and repair kinetics were evaluated by a novel combination of enzyme quantifications, ELISA, specific antagonists of neutrophil enzymes and confocal intravital microscopy. We have demonstrated that neutrophil infiltration is not only involved in injury amplification, but also in liver tissue repair after APAP-induced liver injury. In fact, while neutrophil depletion led to reduced hepatic necrosis during APAP poisoning, injury recovery was also delayed in neutropenic mice. The mechanisms underlying the neutrophil reparative role involved rapid degranulation and matrix metalloproteinases (MMPs) activity. Our data highlights the crucial role of neutrophils, in particular for MMPs, in the resolution phase of APAP-induced inflammatory response