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 | Acesso ao texto completo restrito à biblioteca da Embrapa Hortaliças. Para informações adicionais entre em contato com cnph.biblioteca@embrapa.br. |
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Registro Completo |
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Biblioteca(s): |
Embrapa Cerrados; Embrapa Hortaliças. |
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Data corrente: |
05/02/2009 |
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Data da última atualização: |
05/02/2009 |
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Tipo da produção científica: |
Artigo em Periódico Indexado |
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Autoria: |
ALCÂNTARA, F. A. de; FURTINI NETO, A. E.; CURI, N.; RESENDE, A. V. de. |
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Afiliação: |
Flávia Aparecida de Alcântara, CNPH; Antônio Eduardo Furtini Neto, UFLA; Nilton Curi, UFLA; Álvaro Vilela de Resende, CPAC. |
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Título: |
Extraction methods for phosphorus and their relationship with soils phosphorus-buffer capacity estimated by the remaining-phosphorus methodology-A pot study with maize. |
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Ano de publicação: |
2008 |
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Fonte/Imprenta: |
Communications in Soil Science and Plant Analysis, New York, v. 39, p. 603-615, 2008. |
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Idioma: |
Inglês |
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Palavras-Chave: |
Mechlich 3; Mechlich1; Olsen; Viabilidade biológica. |
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Thesagro: |
Extração; Fósforo; Milho; Solo; Zea Mays. |
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Categoria do assunto: |
-- |
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Marc: |
LEADER 00819naa a2200253 a 4500
001 1571644
005 2009-02-05
008 2008 bl uuuu u00u1 u #d
100 1 $aALCÂNTARA, F. A. de
245 $aExtraction methods for phosphorus and their relationship with soils phosphorus-buffer capacity estimated by the remaining-phosphorus methodology-A pot study with maize.$h[electronic resource]
260 $c2008
650 $aExtração
650 $aFósforo
650 $aMilho
650 $aSolo
650 $aZea Mays
653 $aMechlich 3
653 $aMechlich1
653 $aOlsen
653 $aViabilidade biológica
700 1 $aFURTINI NETO, A. E.
700 1 $aCURI, N.
700 1 $aRESENDE, A. V. de
773 $tCommunications in Soil Science and Plant Analysis, New York$gv. 39, p. 603-615, 2008.
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Registro original: |
Embrapa Cerrados (CPAC) |
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| Acesso ao texto completo restrito à biblioteca da Embrapa Agricultura Digital. Para informações adicionais entre em contato com cnptia.biblioteca@embrapa.br. |
Registro Completo
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Biblioteca(s): |
Embrapa Agricultura Digital. |
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Data corrente: |
03/01/2014 |
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Data da última atualização: |
07/01/2014 |
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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: |
BRAGHINI, C. A.; NESHICH, I. A. P.; NESHICH, G.; SOARDI, F. C.; MELLO, M. P. de; COSTA, V. P.; VASCONCELLOS, J. P. C. de; MELO, M. B. de. |
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Afiliação: |
CAROLINA AYUMI BRAGHINI, CBMEG/Unicamp; IZABELLA AGOSTINHO PENA NESHICH, CBMEG/Unicamp; GORAN NESHICH, CNPTIA; FERNANDA CAROLINE SOARDI, CBMEG/Unicamp; MARICILDA PALANDI DE MELLO, CBMEG/Unicamp; VITAL PAULINO COSTA, FCM/Unicamp; JOSÉ PAULO CABRAL DE VASCONCELLOS, FCM/Unicamp; MÔNICA BARBOSA DE MELO, CBMEG/Unicamp. |
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Título: |
New mutation in the myocilin gene segregates with juvenile-onset open-angle glaucoma in a Brazilian family |
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Ano de publicação: |
2013 |
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Fonte/Imprenta: |
Gene, Amsterdam, v. 535, n. 1, p. 50-57, July 2013. |
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Idioma: |
Inglês |
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Conteúdo: |
Abstract. Mutations in the myocilin gene (MYOC) account for most cases of autosomal dominant juvenile-onset open-angle glaucoma (JOAG), an earlier and more severe form of POAG. We accessed seven members of a Brazilian JOAG family by clinical and molecular investigation. Four out of seven family members were diagnosed with JOAG. All of these patients presented high intraocular pressure and two of them were bilaterally blind. The disease onset varied from 20 to 30 years old. There was a nine-year-old family member who had not yet manifested the disease, although he was also a carrier of the mutation. Ophthalmologic examination included: evaluation of the visual field and optic disc, intraocular pressure measurement, and gonioscopy. The three exons and intron/exon junctions of the MYOC gene were screened for mutations through direct sequencing of PCR-amplified DNA fragments. Mutation screening revealed an in-frame mutation in the third exon of the MYOC gene: an insertion of six nucleotides between the cDNA positions 1187 and 1188 (c.1187_1188insCCCAGA, p.D395_E396insDP). This mutation presented an autosomal dominant pattern of inheritance, segregating with the disease in four family members for three generations, and it was absent in 60 normal controls. We also performed a computational structure modeling of olfactomedin-like domain of myocilin protein and conducted in silico analysis to predict the structural changes in the myocilin protein due to the presence of the mutation. These findings may be important for future diagnosis of other presymptomatic family members, as well as for the increase of the panel of MYOC mutations and their effects on phenotype. MenosAbstract. Mutations in the myocilin gene (MYOC) account for most cases of autosomal dominant juvenile-onset open-angle glaucoma (JOAG), an earlier and more severe form of POAG. We accessed seven members of a Brazilian JOAG family by clinical and molecular investigation. Four out of seven family members were diagnosed with JOAG. All of these patients presented high intraocular pressure and two of them were bilaterally blind. The disease onset varied from 20 to 30 years old. There was a nine-year-old family member who had not yet manifested the disease, although he was also a carrier of the mutation. Ophthalmologic examination included: evaluation of the visual field and optic disc, intraocular pressure measurement, and gonioscopy. The three exons and intron/exon junctions of the MYOC gene were screened for mutations through direct sequencing of PCR-amplified DNA fragments. Mutation screening revealed an in-frame mutation in the third exon of the MYOC gene: an insertion of six nucleotides between the cDNA positions 1187 and 1188 (c.1187_1188insCCCAGA, p.D395_E396insDP). This mutation presented an autosomal dominant pattern of inheritance, segregating with the disease in four family members for three generations, and it was absent in 60 normal controls. We also performed a computational structure modeling of olfactomedin-like domain of myocilin protein and conducted in silico analysis to predict the structural changes in the myocilin protein due to the presence of the mutation.... Mostrar Tudo |
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Palavras-Chave: |
Análises in silico; In-frame mutation; Juvenile-onset open-angle glaucoma; Mutação genética; Myocilin. |
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Thesagro: |
Glaucoma. |
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Thesaurus NAL: |
Mutation. |
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Categoria do assunto: |
X Pesquisa, Tecnologia e Engenharia |
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Marc: |
LEADER 02547naa a2200289 a 4500
001 1974842
005 2014-01-07
008 2013 bl uuuu u00u1 u #d
100 1 $aBRAGHINI, C. A.
245 $aNew mutation in the myocilin gene segregates with juvenile-onset open-angle glaucoma in a Brazilian family$h[electronic resource]
260 $c2013
520 $aAbstract. Mutations in the myocilin gene (MYOC) account for most cases of autosomal dominant juvenile-onset open-angle glaucoma (JOAG), an earlier and more severe form of POAG. We accessed seven members of a Brazilian JOAG family by clinical and molecular investigation. Four out of seven family members were diagnosed with JOAG. All of these patients presented high intraocular pressure and two of them were bilaterally blind. The disease onset varied from 20 to 30 years old. There was a nine-year-old family member who had not yet manifested the disease, although he was also a carrier of the mutation. Ophthalmologic examination included: evaluation of the visual field and optic disc, intraocular pressure measurement, and gonioscopy. The three exons and intron/exon junctions of the MYOC gene were screened for mutations through direct sequencing of PCR-amplified DNA fragments. Mutation screening revealed an in-frame mutation in the third exon of the MYOC gene: an insertion of six nucleotides between the cDNA positions 1187 and 1188 (c.1187_1188insCCCAGA, p.D395_E396insDP). This mutation presented an autosomal dominant pattern of inheritance, segregating with the disease in four family members for three generations, and it was absent in 60 normal controls. We also performed a computational structure modeling of olfactomedin-like domain of myocilin protein and conducted in silico analysis to predict the structural changes in the myocilin protein due to the presence of the mutation. These findings may be important for future diagnosis of other presymptomatic family members, as well as for the increase of the panel of MYOC mutations and their effects on phenotype.
650 $aMutation
650 $aGlaucoma
653 $aAnálises in silico
653 $aIn-frame mutation
653 $aJuvenile-onset open-angle glaucoma
653 $aMutação genética
653 $aMyocilin
700 1 $aNESHICH, I. A. P.
700 1 $aNESHICH, G.
700 1 $aSOARDI, F. C.
700 1 $aMELLO, M. P. de
700 1 $aCOSTA, V. P.
700 1 $aVASCONCELLOS, J. P. C. de
700 1 $aMELO, M. B. de
773 $tGene, Amsterdam$gv. 535, n. 1, p. 50-57, July 2013.
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Embrapa Agricultura Digital (CNPTIA) |
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