1000 resultados para early thinnings


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v.11:no.6(1952)

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v.9:no.2(1944)

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n.s. no.31(1999)

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v.9:no.3(1945)

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no.8(1924)

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The present study aims to compare the buccal apparatus and gastrointestinal tract of early life stages of Centropomus undecimalis (Bloch, 1792), and relate them to its diet. A total of 190 individuals collected with a channel net in the Catuama estuary (07º40'9.9''S, 34º50'36.7''W), northern coast of the state of Pernambuco, were examined. Morphometrical and meristic data were analyzed for the two initial developmental periods (larval and juvenile). Their digestive tube was morphologically characterized and its content identified. The longest transverse axis of food items was measured, and compared to the standard length (SL) and mouth gape size (D) of the individuals. Body measurement regressions differed significantly (p<0.001) between larvae and juveniles. The stomachs with food content (n=118 individuals) presented a proportion of 62% full and 30% empty (being 8% damaged). They differed in relation to the fullness level and presented a coiled shape when empty. The number of food items in relation to SL and D did not present an evident correlation. Larvae (SL<10 mm) feed on small copepods, while juveniles (SL=11.1 to 64.7 mm) ingest larvae of various decapod species, showing a distinct diet between these initial developmental stages.

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Organs developing as appendages of the ectoderm are initiated from epithelial thickenings called placodes. Their formation is regulated by interactions between the ectoderm and underlying mesenchyme, and several signalling molecules have been implicated as activators or inhibitors of placode formation. Ectodysplasin (Eda) is a unique signalling molecule in the tumour necrosis factor family that, together with its receptor Edar, is necessary for normal development of ectodermal organs both in humans and mice. We have shown previously that overexpression of the Eda-A1 isoform in transgenic mice stimulates the formation of several ectodermal organs. In the present study, we have analysed the formation and morphology of placodes using in vivo and in vitro models in which both the timing and amount of Eda-A1 applied could be varied. The hair and tooth placodes of K14-Eda-A1 transgenic embryos were enlarged, and extra placodes developed from the dental lamina and mammary line. Exposure of embryonic skin to Eda-A1 recombinant protein in vitro stimulated the growth and fusion of placodes. However, it did not accelerate the initiation of the first wave of hair follicles giving rise to the guard hairs. Hence, the function of Eda-A1 appears to be downstream of the primary inductive signal required for placode initiation during skin patterning. Analysis of BrdU incorporation indicated that the formation of the epithelial thickening in early placodes does not involve increased cell proliferation and also that the positive effect of Eda-A1 on placode expansion is not a result of increased cell proliferation. Taken together, our results suggest that Eda-A1 signalling promotes placodal cell fate during early development of ectodermal organs.