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 | Acesso ao texto completo restrito à biblioteca da Embrapa Florestas. Para informações adicionais entre em contato com cnpf.biblioteca@embrapa.br. |
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Registro Completo |
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Biblioteca(s): |
Embrapa Florestas. |
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Data corrente: |
29/10/2003 |
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Data da última atualização: |
15/08/2012 |
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Autoria: |
DOSSA, D.; MONTOYA VILCAHUAMAN, L. J. |
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Afiliação: |
Pesquisadores da Embrapa Florestas. |
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Título: |
As atividades florestal e agroflorestal como alternativas de renda aos produtores rurais. |
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Ano de publicação: |
2002 |
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Fonte/Imprenta: |
In: SEMINÁRIO SUL-BRASILEIRO DE ADMINISTRAÇÃO RURAL: Administração Rural para o Século XXI, 2., 2002, Passo Fundo. Anais. Passo Fundo: Universidade de Passo Fundo, 2002. |
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Páginas: |
p. 127-141 |
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Idioma: |
Português |
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Notas: |
Organizado por Rubens Blum. |
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Palavras-Chave: |
Agroflorestal; Atividade florestal; Produtores rurais. |
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Thesagro: |
Renda. |
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Categoria do assunto: |
-- |
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Marc: |
LEADER 00704nam a2200181 a 4500
001 1307569
005 2012-08-15
008 2002 bl uuuu u00u1 u #d
100 1 $aDOSSA, D.
245 $aAs atividades florestal e agroflorestal como alternativas de renda aos produtores rurais.$h[electronic resource]
260 $aIn: SEMINÁRIO SUL-BRASILEIRO DE ADMINISTRAÇÃO RURAL: Administração Rural para o Século XXI, 2., 2002, Passo Fundo. Anais. Passo Fundo: Universidade de Passo Fundo$c2002
300 $ap. 127-141
500 $aOrganizado por Rubens Blum.
650 $aRenda
653 $aAgroflorestal
653 $aAtividade florestal
653 $aProdutores rurais
700 1 $aMONTOYA VILCAHUAMAN, L. J.
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Embrapa Florestas (CNPF) |
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| Acesso ao texto completo restrito à biblioteca da Embrapa Pantanal. Para informações adicionais entre em contato com cpap.biblioteca@embrapa.br. |
Registro Completo
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Biblioteca(s): |
Embrapa Pantanal. |
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Data corrente: |
11/09/1997 |
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Data da última atualização: |
11/09/1997 |
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Autoria: |
SILVA, R. A. M. S.; RAMIREZ, L.; DAVILA, A. M. R.; VICTORIO, A. M.; PEREIRA, M. E. B. |
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Afiliação: |
EMBRAPA. Centro de Pesquisa Agropecuaria do Pantanal (Corumba, MS). |
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Título: |
The mediation of adoptive transference for protection against Trypanosoma evansi by macrophages and spleen cells. |
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Ano de publicação: |
1996 |
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Fonte/Imprenta: |
Memorias do Instituto Oswaldo Cruz, Rio de Janeiro, v.91, p.106, 1996. Suplemento. |
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Idioma: |
Inglês |
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Conteúdo: |
The importance of phagocytic cells in the resistance of an organism to invasion by infectious agents has been recognized for more than one century, since the times of Elie Metchnikoff. A number of in vivo experiments have indicated a direct relationship between the uptake of antigens by the phagocyte system and the extent of immune response. Several authors have reported that Mos taken from mice infected with BCG could kill T.cruzi more efficiently than normal Mos in vitro. Contrary to diseases caused by stercorarian trypanosomes, African trypanosomosis in accompained by profound general immunosuppression. Experimental infection in mice leads to polyclonal proliferation of B-T, and null cells in the blood, spleen, peritoneum, and bone marrow. According to Grosskinsky and Askonas in experiment with T. brucei where after phagocytosis of parasites. Mos were transferred into uninfected syngenic mice the results indicated that the Mfs were key cells in the mediation of parasite-induced immune dysfunction. Our objective in this study was evaluate the importance of Mfs and spleen cells in the transference of passive immunity to non-immune animals. In experiment l macrophage mediated protection. The experimental and the control group received 2550/ul peritoneal Mo, isolated from immune and non-immune Wistar rats, respectively, pretreated 3 days prior a single intraperiotoneal dose of tioglocolate. After 24 h of Mo transference both groups were infected with 11,4 x 10 6 forms to Trypanosoma evansi. In experiment 2 spleen cells mediated protection. The experimental and the control group received 230/ul of spleen cells isolated from immune and non-immune Wistar rats, respectively. After 24h of spleen cells transference both groups were infected with 11,4 x 10 6 forms of T. evansi. The lifespan of control rats in the experiment 1 was 6 +- 2.8 days. In the experimental rats the lifespan was 32.28 +- 14.39 days. A highly statiscally significant between the 2 groups was observed. All control animals died and in the experimental group 30% survived. The lifespan of control rats in the experiment 2 was 3.6 +- 2.6 days. The lifespan of experimental rats was 42.28 +- 5.4 days. A highly statiscally significant difference between the 2 groups was observed. All control animals died and in the experimental group 28,57% survived. A statistically significant diference was not revealed between lifespans of rats that received Mos versus those that received spleen cells (P>0.05). Contrary to reports of immunessuppresion observed in animals infected by salivarian trypanosomes, we observed immunity confered by Mos and spleen cells in experimental groups. Probably either the presentation of antigen blound to live Mos to the lymphocytes of non-immune rats in both experiments was a highly efficient mode of generating and immune response or the Mfs associated antigen was a highly effective in promoting T-B cell collaboration of non-immune rats in both experiments. MenosThe importance of phagocytic cells in the resistance of an organism to invasion by infectious agents has been recognized for more than one century, since the times of Elie Metchnikoff. A number of in vivo experiments have indicated a direct relationship between the uptake of antigens by the phagocyte system and the extent of immune response. Several authors have reported that Mos taken from mice infected with BCG could kill T.cruzi more efficiently than normal Mos in vitro. Contrary to diseases caused by stercorarian trypanosomes, African trypanosomosis in accompained by profound general immunosuppression. Experimental infection in mice leads to polyclonal proliferation of B-T, and null cells in the blood, spleen, peritoneum, and bone marrow. According to Grosskinsky and Askonas in experiment with T. brucei where after phagocytosis of parasites. Mos were transferred into uninfected syngenic mice the results indicated that the Mfs were key cells in the mediation of parasite-induced immune dysfunction. Our objective in this study was evaluate the importance of Mfs and spleen cells in the transference of passive immunity to non-immune animals. In experiment l macrophage mediated protection. The experimental and the control group received 2550/ul peritoneal Mo, isolated from immune and non-immune Wistar rats, respectively, pretreated 3 days prior a single intraperiotoneal dose of tioglocolate. After 24 h of Mo transference both groups were infected with 11,4 x 10 6 forms to Tryp... Mostrar Tudo |
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Thesaurus NAL: |
Trypanosoma evansi. |
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Categoria do assunto: |
-- |
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Marc: |
LEADER 03571naa a2200181 a 4500
001 1791631
005 1997-09-11
008 1996 bl uuuu u00u1 u #d
100 1 $aSILVA, R. A. M. S.
245 $aThe mediation of adoptive transference for protection against Trypanosoma evansi by macrophages and spleen cells.
260 $c1996
520 $aThe importance of phagocytic cells in the resistance of an organism to invasion by infectious agents has been recognized for more than one century, since the times of Elie Metchnikoff. A number of in vivo experiments have indicated a direct relationship between the uptake of antigens by the phagocyte system and the extent of immune response. Several authors have reported that Mos taken from mice infected with BCG could kill T.cruzi more efficiently than normal Mos in vitro. Contrary to diseases caused by stercorarian trypanosomes, African trypanosomosis in accompained by profound general immunosuppression. Experimental infection in mice leads to polyclonal proliferation of B-T, and null cells in the blood, spleen, peritoneum, and bone marrow. According to Grosskinsky and Askonas in experiment with T. brucei where after phagocytosis of parasites. Mos were transferred into uninfected syngenic mice the results indicated that the Mfs were key cells in the mediation of parasite-induced immune dysfunction. Our objective in this study was evaluate the importance of Mfs and spleen cells in the transference of passive immunity to non-immune animals. In experiment l macrophage mediated protection. The experimental and the control group received 2550/ul peritoneal Mo, isolated from immune and non-immune Wistar rats, respectively, pretreated 3 days prior a single intraperiotoneal dose of tioglocolate. After 24 h of Mo transference both groups were infected with 11,4 x 10 6 forms to Trypanosoma evansi. In experiment 2 spleen cells mediated protection. The experimental and the control group received 230/ul of spleen cells isolated from immune and non-immune Wistar rats, respectively. After 24h of spleen cells transference both groups were infected with 11,4 x 10 6 forms of T. evansi. The lifespan of control rats in the experiment 1 was 6 +- 2.8 days. In the experimental rats the lifespan was 32.28 +- 14.39 days. A highly statiscally significant between the 2 groups was observed. All control animals died and in the experimental group 30% survived. The lifespan of control rats in the experiment 2 was 3.6 +- 2.6 days. The lifespan of experimental rats was 42.28 +- 5.4 days. A highly statiscally significant difference between the 2 groups was observed. All control animals died and in the experimental group 28,57% survived. A statistically significant diference was not revealed between lifespans of rats that received Mos versus those that received spleen cells (P>0.05). Contrary to reports of immunessuppresion observed in animals infected by salivarian trypanosomes, we observed immunity confered by Mos and spleen cells in experimental groups. Probably either the presentation of antigen blound to live Mos to the lymphocytes of non-immune rats in both experiments was a highly efficient mode of generating and immune response or the Mfs associated antigen was a highly effective in promoting T-B cell collaboration of non-immune rats in both experiments.
650 $aTrypanosoma evansi
700 1 $aRAMIREZ, L.
700 1 $aDAVILA, A. M. R.
700 1 $aVICTORIO, A. M.
700 1 $aPEREIRA, M. E. B.
773 $tMemorias do Instituto Oswaldo Cruz, Rio de Janeiro$gv.91, p.106, 1996. Suplemento.
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