69 research outputs found

    DISC1 genetics, biology and psychiatric illness

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    Psychiatric disorders are highly heritable, and in many individuals likely arise from the combined effects of genes and the environment. A substantial body of evidence points towards DISC1 being one of the genes that influence risk of schizophrenia, bipolar disorder and depression, and functional studies of DISC1 consequently have the potential to reveal much about the pathways that lead to major mental illness. Here, we review the evidence that DISC1 influences disease risk through effects upon multiple critical pathways in the developing and adult brain

    Global migration of influenza A viruses in swine

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    The complex and unresolved evolutionary origins of the 2009 H1N1 influenza pandemic exposed major gaps in our knowledge of the global spatial ecology and evolution of influenza A viruses in swine (swIAVs). Here we undertake an expansive phylogenetic analysis of swIAV sequence data and demonstrate that the global live swine trade strongly predicts the spatial dissemination of swIAVs, with Europe and North America acting as sources of viruses in Asian countries. In contrast, China has the world's largest swine population but is not a major exporter of live swine, and is not an important source of swIAVs in neighbouring Asian countries or globally. A meta-population simulation model incorporating trade data predicts that the global ecology of swIAVs is more complex than previously thought, and the United States and China's large swine populations are unlikely to be representative of swIAV diversity in their respective geographic regions, requiring independent surveillance efforts throughout Latin America and Asia.status: publishe

    Epizootic eastern equine encephalitis in the Bragança region of Pará, Brazil (Publicado originalmente em 1962)

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    Ministério da Educação e Saúde. Serviço Especial de Saúde Pública. Instituto Evandro. Belém, PA, Brasil.Ministério da Educação e Saúde. Serviço Especial de Saúde Pública. Instituto Evandro. Belém, PA, Brasil.Ministério da Educação e Saúde. Serviço Especial de Saúde Pública. Instituto Evandro. Belém, PA, Brasil.Ministério da Educação e Saúde. Serviço Especial de Saúde Pública. Instituto Evandro. Belém, PA, Brasil.Uma epizootia de vírus EEE, entre cavalos nas pastagens de Bragança foi estudada em 1960. O vírus foi isolado do Aedes taeniorhynchus de cavalos jovens. Outros animais domésticos, pássaros e animais silvestres foram negativos para o vírus. Anticorpos hemaglutinantes para EEE estavam presentes em cavalos (69%), pássaros (10%), homem (9%) e mucura (5%) Trypanosoma equinum foi isolado de um dos cavalos doentes e vírus de Encephalomyocarditis foi obtido de dois outros

    The epidemiology of EEE, WEE, SLE and Turlock viruses, with special reference to birds, in a tropical rain forest near Belém, Brazil (Publicado originalmente em 1966)

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    Ministério da Saúde. Fundação Serviços de Especial de Saúde Pública. Instituto Evandro Chagas. Laboratório de Vírus de Belém. Belém, PA, Brasil.Ministério da Saúde. Fundação Serviços de Especial de Saúde Pública. Instituto Evandro Chagas. Laboratório de Vírus de Belém. Belém, PA, Brasil.Ministério da Saúde. Fundação Serviços de Especial de Saúde Pública. Instituto Evandro Chagas. Laboratório de Vírus de Belém. Belém, PA, Brasil.Ministério da Saúde. Fundação Serviços de Especial de Saúde Pública. Instituto Evandro Chagas. Laboratório de Vírus de Belém. Belém, PA, Brasil.Smithsonian Institution. Washington, D.C., USATwo thousand sixty-eight forest and open-field birds captured near Belém, Brazil, in 1963 and 1964 were tested for the presence of arboviruses, and 1,462 of the birds were tested for antibody using 25 viruses. Strains of Western Equine Encephalitis (WEE), St. Louis Encephalitis (SLE) and Turlock viruses were isolated from forest birds in 1964. There were forest birds with hemagglutination-inhibiting and neutralizing substance for Eastern Equine Encephalitis (EEE) virus in 1963 and for EEE, WEE, SLE and Turlock viruses in 1964. Antibody rates were much higher in forest birds than in open-field birds. In 1964 more than half the antibody detected for WEE, SLE and Turlock viruses was found in Coragyps atratus and birds of the family Formicariidae. There was little antibody for EEE, WEE, SLE or Turlock virus in forest rodents or marsupials. EEE virus was isolated from five pools of Culex (Melanoconion) taeniopus in 1963, 1964 and 1965. SLE virus was isolated from ground-foliage Culex (Culex) sp. (probably virgultus) in 1964. Possible cycles of EEE, WEE, SLE and Turlock viruses in the forest of the Instituto de Pesquisas e Experimentação Agropecuarias do Norte are discussed

    Aging-induced proteostatic changes in the rat hippocampus identify ARP3, NEB2 and BRAG2 as a molecular circuitry for cognitive impairment

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    Disturbed proteostasis as a particular phenotype of the aging organism has been advanced in C. elegans experiments and is also conceived to underlie neurodegenerative diseases in humans. Here, we investigated whether particular changes in non-disease related proteostasis can be identified in the aged mammalian brain, and whether a particular signature of aberrant proteostasis is related to behavioral performance of learning and memory. Young (adult, n = 30) and aged (2 years, n = 50) Wistar rats were tested in the Morris Water Maze (MWM) to distinguish superior and inferior performers. For both young and old rats, the best and worst performers in the MWM were selected and the insoluble proteome, termed aggregome, was purified from the hippocampus as evidence for aberrant proteostasis. Quantitative proteomics (iTRAQ) was performed. The aged inferior performers were considered as a model for spontaneous, age-associated cognitive impairment. Whereas variability of the insoluble proteome increased with age, absolute changes in the levels of insoluble proteins were small compared to the findings in the whole C. elegans insoluble proteome. However, we identified proteins with aberrant proteostasis in aging. For the cognitively impaired rats, we identified a changed molecular circuitry of proteins selectively involved in F-actin remodeling, synapse building and long-term depression: actin related protein 3 (ARP3), neurabin II (NEB2) and IQ motif and SEC7 domain-containing protein 1 (BRAG2). We demonstrate that aberrant proteostasis is a specific phenotype of brain aging in mammals. We identify a distinct molecular circuitry where changes in proteostasis are characteristic for poor learning and memory performance in the wild type, aged rat. Our findings 1. establish the search for aberrant proteostasis as a successful strategy to identify neuronal dysfunction in deficient cognitive behavior, 2. reveal a previously unknown functional network of proteins (ARP3, NEB2, BRAG2) involved in age-associated cognitive dysfunction. © 2013 Ottis et al
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