Assuntos
Transtornos do Crescimento/diagnóstico por imagem , Transtornos do Crescimento/genética , Determinação da Idade pelo Esqueleto , Estatura , Desenvolvimento Ósseo , Criança , Feminino , Proteínas de Homeodomínio/genética , Humanos , Osteocondrodisplasias/diagnóstico por imagem , Osteocondrodisplasias/genética , Proteína de Homoeobox de Baixa Estatura , Síndrome , Fatores de Transcrição/genéticaRESUMO
The present study demonstrates that farmed Atlantic salmon, Salmo salar, health is positively and significantly affected by synergistic effects between very long-chain polyunsaturated fatty acids of the n-3 family eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) and iron, where positive effects of high dietary levels of EPA/DHA are enhanced when combined with low levels of iron. Based on cumulative mortalities in the different experimental groups, relative percentage of survival (RPS) for the high EPA/DHA-low iron group was 70% during an outbreak of furunculosis and 96% during an outbreak of cold water vibriosis compared with the controls. A non-additive effect between EPA/DHA and iron was confirmed by statistical analyses that revealed a significant effect of EPA/DHA alone and an interaction of iron with EPA/DHA. Liver cell cultures treated with EPA/DHA revealed that the synergistic effect could be related to an EPA/DHA dependent regulation of mRNA for proteins important for transport (transferrin) and storage (ferritin) of iron in the salmon. In keeping with this finding, the transcriptional down-regulation of iron metabolism in vitro was reflected in decreased in vivo iron stores with increasing levels of dietary EPA/DHA. Hence, to avoid overloading of the iron transport/storage-systems resulting in increased susceptibility to bacterial infections, high levels of dietary EPA/DHA should be accompanied by low levels of dietary iron.
Assuntos
Ácidos Graxos Ômega-3/administração & dosagem , Doenças dos Peixes/dietoterapia , Furunculose/veterinária , Ferro da Dieta/administração & dosagem , Salmo salar , Vibrioses/veterinária , Animais , Ácidos Docosa-Hexaenoicos/administração & dosagem , Sinergismo Farmacológico , Ácido Eicosapentaenoico/administração & dosagem , Ferritinas/genética , Doenças dos Peixes/mortalidade , Furunculose/dietoterapia , Furunculose/mortalidade , RNA Mensageiro/análise , Taxa de Sobrevida , Transferrina/genética , Vibrioses/dietoterapia , Vibrioses/mortalidadeRESUMO
Introducción: El síndrome de West (SW) se caracteriza por la presencia de espasmos en salvas, trazado electroencefalográfico hipsarrítmico y detención o regresión en el desarrollo psicomotor. El objetivo de este estudio es conocer la distribución etiológica del SW en nuestro medio y su evolución en el tiempo. Método: Estudio retrospectivo de 20 niños diagnosticados de SW entre 1993 y 2001. Se analizan las causas y se describen los métodos diagnósticos empleados, tratamiento y evolución. Se comparan los resultados con otro estudio realizado entre 1975 y 1986 en el mismo hospital. Resultados: Relación varón:mujer de 1,5:1. La edad media al comenzar los espasmos fue de 7,4 meses (rango 2-14 meses), con una demora hasta el diagnóstico igual o superior al mes en el 60 por ciento de los casos. Se identificaron 16 casos sintomáticos (11 de origen prenatal, 4 perinatal y 1 postnatal), 3 criptogénicos y 1 idiopático. La hipsarritmia y los espasmos desaparecieron en todos los pacientes, pero en la mitad de los casos sintomáticos persistieron otros tipos de crisis. Se registraron 3 exitus, todos sintomáticos. La proporción de casos sintomáticos fue significativamente mayor en el período 1993-2001 (16/20, 80 por ciento) respecto a 1975-1986 (15/30, 50 por ciento). Conclusiones: Las nuevas tecnologías permiten identificar como sintomáticos una mayor proporción de pacientes con SW. Persiste una importante demora en el diagnóstico por la confusión de los 'espasmos' con otros episodios paroxísticos no epilépticos. Ante la sospecha clínica debe practicarse un electroencefalograma con urgencia para confirmar o descartar hipsarritmia. Las lesiones preexistentes condicionan la evolución de los SW sintomáticos (AU)
Assuntos
Feminino , Lactente , Masculino , Humanos , Espasmos Infantis/etiologia , Eletroencefalografia , Recém-Nascido de muito Baixo Peso , Recém-Nascido Prematuro , Transtornos Psicomotores/complicações , Esclerose Tuberosa/complicações , Ácido Valproico/uso terapêutico , Cosintropina/uso terapêutico , Vigabatrina/uso terapêutico , Espasmos Infantis/tratamento farmacológicoRESUMO
A cDNA fragment which encodes salmon peroxisome proliferator activated receptor y (sPPARgamma) was amplified by PCR from the liver of Atlantic salmon (Salmo salar L.). The fragment was 627 bp long. The sequence of the amplified PCR product was similar to the PPARgamma of mouse and hamster. 59% of the bases were identical. Northern blot analysis of salmon liver mRNA showed that the amplified sPPARgamma fragment hybridised to three specific transcripts of lengths 1.6, 2.4 and 3.3 kb. Clofibric acid and bezafibrate, administered to salmon hepatocytes in culture, resulted in a 1.7-fold increase of the 1.6 kb sPPARgamma transcript. The activity of acyl-CoA oxidase also increased approx. 1.7-fold after administration of fibrates. These results indicate that PPAR is an important factor in mediating enzymatic response to fibrates in fish.
Assuntos
Ácidos Graxos/farmacologia , Fígado/efeitos dos fármacos , Microcorpos/efeitos dos fármacos , Oxirredutases/metabolismo , Receptores Citoplasmáticos e Nucleares/genética , Salmão , Fatores de Transcrição/genética , Acil-CoA Oxidase , Animais , Sequência de Bases , Bezafibrato/farmacologia , Northern Blotting , Clofibrato/farmacologia , DNA Complementar/análise , DNA Complementar/química , Humanos , L-Lactato Desidrogenase/metabolismo , Fígado/metabolismo , Fígado/ultraestrutura , Microcorpos/enzimologia , Dados de Sequência Molecular , Reação em Cadeia da Polimerase , Análise de Sequência de DNA , Homologia de Sequência , Transcrição Gênica/efeitos dos fármacosRESUMO
Transferrin mRNA in liver was quantified in farmed Atlantic salmon (Salmo salar) fed three different levels (310-, 65-, and 40 ppm) of dietary iron for 26 weeks. At the time of sampling, the fish fed 40 ppm iron showed symptoms of iron deficiency. Mean values of liver storage iron was reduced from 84 to 12 mg kg(-1) and plasma iron from 2.3 to 1.6 mg l(-1) compared with fish fed 310 ppm iron. No significant difference in transferrin mRNA was observed between normal and iron deficient salmon; the amount of Tf mRNA was not related to the amount of stored iron, either in groups or individual fish. This suggests that there is no iron-modulated transcriptional regulation of liver Tf expression in salmon as there is in chickens and rats.
RESUMO
The ferritin heavy (H) and middle (M) subunit cDNAs were isolated from the Atlantic salmon (Salmo salar) liver. Full-length clones encoding the ferritin M subunit of 176 residues were obtained by screening of a liver cDNA library. The evolutionary conserved iron-responsive element (IRE) was identified in the upstream untranslated region. Ferritin H cDNA was cloned by running reverse transcription-polymerase chain reaction (RT-PCR) on salmon liver mRNA. The salmon ferritin H subunit of 177 residues showed 67% sequence identity with the M subunit. Northern blot analysis revealed ferritin H mRNA in the liver, gonads, head kidney, heart, and spleen, whereas M subunit mRNA was found almost exclusively in the gonads. Polyclonal antibodies against both salmon ferritin H and M were raised in rabbits.