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Registro Completo |
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Biblioteca(s): |
Embrapa Caprinos e Ovinos. |
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Data corrente: |
04/11/1998 |
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Data da última atualização: |
04/11/1998 |
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Autoria: |
MORAES, J. C. F.; SOUZA, C. J. H. de; COLLARES, R. S. |
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Título: |
Situacao atual e perspectivas da inseminacao artificial em ovinos. |
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Ano de publicação: |
1998 |
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Fonte/Imprenta: |
Revista Brasileira de Reproducao Animal, v.22, n.2, p.87-91, 1998. |
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Idioma: |
Português |
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Conteúdo: |
O objetivo e de apresentar um breve historico da IA em ovinos, os resultados de um levantamento do nivel de adocao nos anos 90, o potencial beneficio economico e uma analise critica das perspectivas futuras da IA na producao. |
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Palavras-Chave: |
Brasil. |
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Thesagro: |
Inseminação Artificial; Ovino. |
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Thesaurus Nal: |
artificial insemination; Brazil; sheep. |
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Categoria do assunto: |
-- |
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Marc: |
LEADER 00822naa a2200217 a 4500
001 1518641
005 1998-11-04
008 1998 bl uuuu u00u1 u #d
100 1 $aMORAES, J. C. F.
245 $aSituacao atual e perspectivas da inseminacao artificial em ovinos.
260 $c1998
520 $aO objetivo e de apresentar um breve historico da IA em ovinos, os resultados de um levantamento do nivel de adocao nos anos 90, o potencial beneficio economico e uma analise critica das perspectivas futuras da IA na producao.
650 $aartificial insemination
650 $aBrazil
650 $asheep
650 $aInseminação Artificial
650 $aOvino
653 $aBrasil
700 1 $aSOUZA, C. J. H. de
700 1 $aCOLLARES, R. S.
773 $tRevista Brasileira de Reproducao Animal$gv.22, n.2, p.87-91, 1998.
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Registro original: |
Embrapa Caprinos e Ovinos (CNPC) |
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 | Acesso ao texto completo restrito à biblioteca da Embrapa Gado de Leite. Para informações adicionais entre em contato com cnpgl.biblioteca@embrapa.br. |
Registro Completo
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Biblioteca(s): |
Embrapa Gado de Leite. |
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Data corrente: |
16/01/2014 |
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Data da última atualização: |
09/02/2024 |
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Tipo da produção científica: |
Artigo em Periódico Indexado |
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Circulação/Nível: |
A - 2 |
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Autoria: |
RODRIGUES, M. F.; ALVES, C. C. S.; FIGUEIREDO, B. B. M.; REZENDE, A. B.; WOHLRES-VIANA, S.; SILVA, V. L.; MACHADO, M. A.; TEIXEIRA, H. C. |
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Afiliação: |
MICHELE F. RODRIGUES, UFJF; CAIO C. S. ALVES, UFJF; BÁRBARA B. M. FIGUEIREDO, UFJF; ALICE B. REZENDE, UFJF; SABINE WOHLRES-VIANA, UFJF; VANIA LUCIA DA SILVA, UFJF; MARCO ANTONIO MACHADO, CNPGL; HENRIQUE C. TEIXEIRA, UFJF. |
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Título: |
Tumour necrosis factor receptors and apoptosis of alveolar macrophages during early infection with attenuaed and virulent Mycobacterium bovis. |
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Ano de publicação: |
2013 |
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Fonte/Imprenta: |
Immunology, v. 139, n. 4, p. 503-512, 2013. |
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DOI: |
https://doi.org/10.1111%2Fimm.12097 |
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Idioma: |
Inglês |
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Conteúdo: |
Apoptosis of macrophages has been reported as an effective host strategy to control the growth of intracellular pathogens, including pathogenic mycobacteria. Tumour necrosis factor-α (TNF-α) plays an important role in the modulation of apoptosis of infected macrophages. It exerts its biological activities via two distinct cell surface receptors, TNFR1 and TNFR2, whose extracellular domain can be released by proteolysis forming soluble TNF receptors (sTNFR1 and sTNFR2). The signalling through TNFR1 initiates the majority of the biological functions of TNF-α, leading to either cell death or survival whereas TNFR2 mediates primarily survival signals. Here, the expression of TNF-α receptors and the apoptosis of alveolar macrophages were investigated during the early phase of infection with attenuated and virulent mycobacteria in mice. A significant increase of apoptosis and high expression of TNFR1 were observed in alveolar macrophages at 3 and 7 days after infection with attenuated Mycobacterium bovis but only on day 7 in infection with the virulent M. bovis. Low surface expression of TNFR1 and increased levels of sTNFR1 on day 3 after infection by the virulent strain were associated with reduced rates of apoptotic macrophages. In addition, a significant reduction in apoptosis of alveolar macrophages was observed in TNFR1−/− mice at day 3 after bacillus Calmette–Guérin infection. These results suggest a potential role for TNFR1 in mycobacteria-induced alveolar macrophage apoptosis in vivo. In this scenario, shedding of TNFR1 seems to contribute to the modulation of macrophage apoptosis in a strain-dependent manner. MenosApoptosis of macrophages has been reported as an effective host strategy to control the growth of intracellular pathogens, including pathogenic mycobacteria. Tumour necrosis factor-α (TNF-α) plays an important role in the modulation of apoptosis of infected macrophages. It exerts its biological activities via two distinct cell surface receptors, TNFR1 and TNFR2, whose extracellular domain can be released by proteolysis forming soluble TNF receptors (sTNFR1 and sTNFR2). The signalling through TNFR1 initiates the majority of the biological functions of TNF-α, leading to either cell death or survival whereas TNFR2 mediates primarily survival signals. Here, the expression of TNF-α receptors and the apoptosis of alveolar macrophages were investigated during the early phase of infection with attenuated and virulent mycobacteria in mice. A significant increase of apoptosis and high expression of TNFR1 were observed in alveolar macrophages at 3 and 7 days after infection with attenuated Mycobacterium bovis but only on day 7 in infection with the virulent M. bovis. Low surface expression of TNFR1 and increased levels of sTNFR1 on day 3 after infection by the virulent strain were associated with reduced rates of apoptotic macrophages. In addition, a significant reduction in apoptosis of alveolar macrophages was observed in TNFR1−/− mice at day 3 after bacillus Calmette–Guérin infection. These results suggest a potential role for TNFR1 in mycobacteria-induced alveolar macrophage apopto... Mostrar Tudo |
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Palavras-Chave: |
Apoptose; Macrófagos; Receptor do fator de necrose tumoral. |
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Thesagro: |
Mycobacterium Bovis. |
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Categoria do assunto: |
L Ciência Animal e Produtos de Origem Animal |
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Marc: |
LEADER 02510naa a2200265 a 4500
001 1976421
005 2024-02-09
008 2013 bl uuuu u00u1 u #d
024 7 $ahttps://doi.org/10.1111%2Fimm.12097$2DOI
100 1 $aRODRIGUES, M. F.
245 $aTumour necrosis factor receptors and apoptosis of alveolar macrophages during early infection with attenuaed and virulent Mycobacterium bovis.$h[electronic resource]
260 $c2013
520 $aApoptosis of macrophages has been reported as an effective host strategy to control the growth of intracellular pathogens, including pathogenic mycobacteria. Tumour necrosis factor-α (TNF-α) plays an important role in the modulation of apoptosis of infected macrophages. It exerts its biological activities via two distinct cell surface receptors, TNFR1 and TNFR2, whose extracellular domain can be released by proteolysis forming soluble TNF receptors (sTNFR1 and sTNFR2). The signalling through TNFR1 initiates the majority of the biological functions of TNF-α, leading to either cell death or survival whereas TNFR2 mediates primarily survival signals. Here, the expression of TNF-α receptors and the apoptosis of alveolar macrophages were investigated during the early phase of infection with attenuated and virulent mycobacteria in mice. A significant increase of apoptosis and high expression of TNFR1 were observed in alveolar macrophages at 3 and 7 days after infection with attenuated Mycobacterium bovis but only on day 7 in infection with the virulent M. bovis. Low surface expression of TNFR1 and increased levels of sTNFR1 on day 3 after infection by the virulent strain were associated with reduced rates of apoptotic macrophages. In addition, a significant reduction in apoptosis of alveolar macrophages was observed in TNFR1−/− mice at day 3 after bacillus Calmette–Guérin infection. These results suggest a potential role for TNFR1 in mycobacteria-induced alveolar macrophage apoptosis in vivo. In this scenario, shedding of TNFR1 seems to contribute to the modulation of macrophage apoptosis in a strain-dependent manner.
650 $aMycobacterium Bovis
653 $aApoptose
653 $aMacrófagos
653 $aReceptor do fator de necrose tumoral
700 1 $aALVES, C. C. S.
700 1 $aFIGUEIREDO, B. B. M.
700 1 $aREZENDE, A. B.
700 1 $aWOHLRES-VIANA, S.
700 1 $aSILVA, V. L.
700 1 $aMACHADO, M. A.
700 1 $aTEIXEIRA, H. C.
773 $tImmunology$gv. 139, n. 4, p. 503-512, 2013.
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