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Registro Completo |
Biblioteca(s): |
Embrapa Florestas; Embrapa Pantanal. |
Data corrente: |
16/08/2011 |
Data da última atualização: |
12/08/2014 |
Tipo da produção científica: |
Documentos |
Autoria: |
MATTOS, P. P. de; BRAZ, E. M.; HESS, A. F.; SALIS, S. M. de. |
Afiliação: |
PATRICIA POVOA DE MATTOS, CNPF; EVALDO MUNOZ BRAZ, CNPF; ANDRÉ FELIPE HESS, UFSC; SUZANA MARIA DE SALIS, CPAP. |
Título: |
A dendrocronologia e o manejo florestal sustentável em florestas tropicais. |
Ano de publicação: |
2011 |
Fonte/Imprenta: |
Colombo : Embrapa Florestas; Corumbá : Embrapa Pantanal, 2011. |
Páginas: |
37 p. |
Série: |
(Embrapa Florestas. Documentos, 218; Embrapa Pantanal. Documentos, 112). |
Idioma: |
Português |
Palavras-Chave: |
Dendrocronologia; Manejo florestal; Sustentabilidade. |
Thesagro: |
Dendrologia; Espécie nativa; Manejo. |
Categoria do assunto: |
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URL: |
https://ainfo.cnptia.embrapa.br/digital/bitstream/item/40456/1/Doc218.pdf
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Marc: |
LEADER 00708nam a2200229 a 4500 001 1898053 005 2014-08-12 008 2011 bl uuuu u0uu1 u #d 100 1 $aMATTOS, P. P. de 245 $aA dendrocronologia e o manejo florestal sustentável em florestas tropicais. 260 $aColombo : Embrapa Florestas; Corumbá : Embrapa Pantanal$c2011 300 $a37 p. 490 $a(Embrapa Florestas. Documentos, 218; Embrapa Pantanal. Documentos, 112). 650 $aDendrologia 650 $aEspécie nativa 650 $aManejo 653 $aDendrocronologia 653 $aManejo florestal 653 $aSustentabilidade 700 1 $aBRAZ, E. M. 700 1 $aHESS, A. F. 700 1 $aSALIS, S. M. de
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Embrapa Florestas (CNPF) |
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| Acesso ao texto completo restrito à biblioteca da Embrapa Recursos Genéticos e Biotecnologia. Para informações adicionais entre em contato com cenargen.biblioteca@embrapa.br. |
Registro Completo
Biblioteca(s): |
Embrapa Recursos Genéticos e Biotecnologia. |
Data corrente: |
07/12/2015 |
Data da última atualização: |
20/03/2023 |
Tipo da produção científica: |
Artigo em Periódico Indexado |
Circulação/Nível: |
A - 1 |
Autoria: |
PETRIZ, B. A.; ALMEIDA, J. A.; GOMES, C. P. C.; PEREIRA, R. W.; MURAD, A. M.; FRANCO, O. L. |
Afiliação: |
Bernardo A. Petriz, UCB; Jeeser A. Almeida, UCB; Clarissa P. C. Gomes, UCB; Rinaldo W. Pereira, UCB; ANDRE MELRO MURAD, CENARGEN; Octavio l. Franco, UCB. |
Título: |
NanoUPLC/MSE proteomic analysis reveals modulation on left ventricle proteome from hypertensive rats after exercise training. |
Ano de publicação: |
2015 |
Fonte/Imprenta: |
Journal of Proteomics, v. 113, p. 351-365, 2015. |
Idioma: |
Inglês |
Conteúdo: |
NanoUPLC/MSE was used to verify the effects of 8 weeks of low (SHR-LIT = 4) and high (SHR-HIT = 4) intensity training over the left ventricle proteome of hypertensive rats (SHR-C = 4). Training enhanced the aerobic capacity and reduced the systolic blood pressure in all exercised rats.NanoUPLC/MSE identified 250 proteins, with 233 in common to all groups and 16 exclusive to SHR-C, 2 to SHR-LIT, and 2 to the SHR-HIT. Cardiac hypertrophy related proteins appeared only in SHR-C. The SHR-LIT enhanced the abundance of 30 proteins and diminished 6, while SHR-HIT enhanced the abundance of 39 proteins and reduced other 7. The levels of metabolic (? and ?-enolase, adenine phosphoribosultransferase, and cytochrome b-c1), myofibril (myosin light chain 4, tropomyosin ? and ?-chain), and transporter proteins (hemoglobin, serum albumin, and hemopexin)were increased by both intensities. Transcription regulator and histone variants were enhanced by SHR-LIT and SHR-HIT respectively. SHR-LIT reduced the concentration of myosin binding protein C, while desmin and membrane voltage dependent anion selective channel protein-3 were reduced only by SHR-HIT. In addition, polyubiquitin B and C, and transcription regulators decreased in both intensities. Exercise also increased the concentration of anti-oxidant proteins, peroxiredozin-6 and glutathione peroxidase-1. Biological significance Pathologic left ventricle hypertrophy if one of the major outcomes of hypertension being a strong predictor of heart failure. Among the various risk factors for cardiovascular disorders, arterial hypertension is responsible for the highest rates of mortality worldwide. In this way,this present study contribute to the understanding of the molecular mechanisms involved in the attenuation of hypertension and the regression of pathological cardiac hypertrophy induced by exercise training. MenosNanoUPLC/MSE was used to verify the effects of 8 weeks of low (SHR-LIT = 4) and high (SHR-HIT = 4) intensity training over the left ventricle proteome of hypertensive rats (SHR-C = 4). Training enhanced the aerobic capacity and reduced the systolic blood pressure in all exercised rats.NanoUPLC/MSE identified 250 proteins, with 233 in common to all groups and 16 exclusive to SHR-C, 2 to SHR-LIT, and 2 to the SHR-HIT. Cardiac hypertrophy related proteins appeared only in SHR-C. The SHR-LIT enhanced the abundance of 30 proteins and diminished 6, while SHR-HIT enhanced the abundance of 39 proteins and reduced other 7. The levels of metabolic (? and ?-enolase, adenine phosphoribosultransferase, and cytochrome b-c1), myofibril (myosin light chain 4, tropomyosin ? and ?-chain), and transporter proteins (hemoglobin, serum albumin, and hemopexin)were increased by both intensities. Transcription regulator and histone variants were enhanced by SHR-LIT and SHR-HIT respectively. SHR-LIT reduced the concentration of myosin binding protein C, while desmin and membrane voltage dependent anion selective channel protein-3 were reduced only by SHR-HIT. In addition, polyubiquitin B and C, and transcription regulators decreased in both intensities. Exercise also increased the concentration of anti-oxidant proteins, peroxiredozin-6 and glutathione peroxidase-1. Biological significance Pathologic left ventricle hypertrophy if one of the major outcomes of hypertension being a strong predictor of he... Mostrar Tudo |
Palavras-Chave: |
Análise proteômica; Hipertensão. |
Categoria do assunto: |
-- |
Marc: |
LEADER 02514naa a2200205 a 4500 001 2030868 005 2023-03-20 008 2015 bl uuuu u00u1 u #d 100 1 $aPETRIZ, B. A. 245 $aNanoUPLC/MSE proteomic analysis reveals modulation on left ventricle proteome from hypertensive rats after exercise training.$h[electronic resource] 260 $c2015 520 $aNanoUPLC/MSE was used to verify the effects of 8 weeks of low (SHR-LIT = 4) and high (SHR-HIT = 4) intensity training over the left ventricle proteome of hypertensive rats (SHR-C = 4). Training enhanced the aerobic capacity and reduced the systolic blood pressure in all exercised rats.NanoUPLC/MSE identified 250 proteins, with 233 in common to all groups and 16 exclusive to SHR-C, 2 to SHR-LIT, and 2 to the SHR-HIT. Cardiac hypertrophy related proteins appeared only in SHR-C. The SHR-LIT enhanced the abundance of 30 proteins and diminished 6, while SHR-HIT enhanced the abundance of 39 proteins and reduced other 7. The levels of metabolic (? and ?-enolase, adenine phosphoribosultransferase, and cytochrome b-c1), myofibril (myosin light chain 4, tropomyosin ? and ?-chain), and transporter proteins (hemoglobin, serum albumin, and hemopexin)were increased by both intensities. Transcription regulator and histone variants were enhanced by SHR-LIT and SHR-HIT respectively. SHR-LIT reduced the concentration of myosin binding protein C, while desmin and membrane voltage dependent anion selective channel protein-3 were reduced only by SHR-HIT. In addition, polyubiquitin B and C, and transcription regulators decreased in both intensities. Exercise also increased the concentration of anti-oxidant proteins, peroxiredozin-6 and glutathione peroxidase-1. Biological significance Pathologic left ventricle hypertrophy if one of the major outcomes of hypertension being a strong predictor of heart failure. Among the various risk factors for cardiovascular disorders, arterial hypertension is responsible for the highest rates of mortality worldwide. In this way,this present study contribute to the understanding of the molecular mechanisms involved in the attenuation of hypertension and the regression of pathological cardiac hypertrophy induced by exercise training. 653 $aAnálise proteômica 653 $aHipertensão 700 1 $aALMEIDA, J. A. 700 1 $aGOMES, C. P. C. 700 1 $aPEREIRA, R. W. 700 1 $aMURAD, A. M. 700 1 $aFRANCO, O. L. 773 $tJournal of Proteomics$gv. 113, p. 351-365, 2015.
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