Navegando por Assunto "Galinha"

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Alterações hematológicas, bioquímicas e histopatológicas no modelo de malária aviária Gallus gallus por Plasmodium gallinaceum: papel do óxido nítrico
(Universidade Federal do Pará, 2011-07-29) MACCHI, Barbarella de Matos; DAMATTA, Renato Augusto; http://lattes.cnpq.br/6212140983414786; NASCIMENTO, José Luiz Martins do; http://lattes.cnpq.br/7216249286784978
Malaria causes major losses to human populations in the world. Experimental models are needed for a better understanding of the pathological mechanisms of the diseases and the development of new treatments. Chickens infected with Plasmodium gallinaceum constitute an adequate malaria model due to the phylogenetic proximity of this parasite to human Plasmodium as well as similarities in disease manifestation, as cerebral malaria. The aim of the present study was to investigate the role of nitric oxide in avian malaria development in chickens experimentally infected with P. gallinaceum, treated or not with aminoguanidine (AG - nitric oxide synthase inhibitor). Survival, classical hematology, serum biochemistry and pathology was assayed during the development of the disease. The greatest survival was observed in animals treated with AG that also presented higher parasitemia. Decrease in hematological parameters and Mean Corspucular Volume of erythrocytes increase was showed, indicating bone marrow response to anemia. Lymphopenia and thrombocytopenia were detected in infected animals, but not at the same proportion in treated animals. Monocytes, lymphocytes and heterophils showed an increase in size and changes that indicated activation. Thrombocytes were also higher with the infection and with atypical morphology. Treated animals showed fewer lesions in histological sections of brain, liver and spleen, and NO production decreased, principally during high parasitemia, compared to untreated animals. These results characterize the participation of the chemistry mediator nitric oxide in the pathogenesis of malaria in the avian model.
Desconhecido
Efeitos do fator de crescimento do nervo sobre os níveis extracelulares de glutamato e compostos tióis na retina embrionária de galinha
(Universidade Federal do Pará, 2011-04-20) GARCIA, Tarcyane Barata; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247
Nerve growth factor (NGF) belongs to the neurotrophin family and induces its effects through activation of two distinct receptor types. NGF was first described by Rita Levi-Montalcini and collaborators as an important factor involved in nerve differentiation and survival. Another role for NGF has been established in neurotransmitter release in the hippocampus, developing visual cortex and cerebellar neuron. However, this phenomenon has not been demonstrated in retina to date. We therefore investigated whether NGF can modulate the glutamate release in the retinal tissue at its peak of the neurotrophic activity (E10-E12). In addition this, we aimed to study the mechanisms of this effect about its dependence on extracellular Ca2+ and participation of Na+-dependent and Na+-independent glutamate transporters. Since high levels of glutamate signalization have been implicated in the oxidative stress, we also investigated the effects of NGF on the thiols compounds. We used intact retinal tissue from chicken embryos (E11) incubated with NGF (10, 50, 100 ng/ml) for different periods (15, 30, 45, 60, 120 min). Extracellular glutamate and thiols content was measured by HPLC methods and colorimetric assay, respectively. We found that NGF rapidly enhances the release of basal glutamate and it can induce thiol release in a more prolonged time of incubation, as well. Interestingly, the NGF-induced increase in the extracellular levels of glutamate was blocked by Ca2+-free medium only in retina treated for 15 min. Retina incubated for 30 min showed a non-vesicular NGF-induced glutamate release. Since glutamate and thiol release was not blocked by Zn2+, we suggested the possible involvement of system Xc- in both processes.NGF-induced increase in the extracellular thiol could be an important protective mechanism enabling retinal neurons to maintain their redox status during development.