999 resultados para X.500
Resumo:
The genus Thalassa Mulsant, 1850 is revised. Its five species are redescribed: T. pentaspilota (Chevrolat, 1853), T. flaviceps Mulsant, 1850, T. similaris Mulsant, 1850, T. montezumae Mulsant, 1850, and T. glauca (Mulsant, 1850). A new species is proposed, Thalassa korschefskyi sp.nov., from Colombia. The species are illustrated and a key to species is also provided. Lectotype of Thalassa reyi Mulsant, 1850 is here designated.
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The current study examined the coparenting and toddler's interactive styles in family coalitions. According to structural family theory, boundaries between generations are clear in alliances, but disturbed in coalitions: the parents look to the child to regulate their conflictual relationship and the child attempts to meet this need. In a normative sample studied longitudinally during the Lausanne Trilogue Play situation (LTP, N=38), 15 coalition cases were detected. Styles of coparenting and of child's interactions were determined and compared in coalition and alliance cases at 18 months. Findings confirm the structural family model by showing the specific ways in which the coparenting and the toddler's interactive styles are associated in 3 different patterns of coalitions: binding, detouring, and triangulation. They illustrate how the child's triangular capacity, or her ability to simultaneously communicate with both parents, is used to regulate the parents' relationship. They suggest that the LTP observational paradigm is a promising assessment method of early family interactions. They point to the importance of assessing early the child's contribution to family coalitions.
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Mutations in the epithelial morphogen ectodysplasin-A (EDA), a member of the tumor necrosis factor (TNF) family, are responsible for the human disorder X-linked hypohidrotic ectodermal dysplasia (XLHED) characterized by impaired development of hair, eccrine sweat glands, and teeth. EDA-A1 and EDA-A2 are two splice variants of EDA, which bind distinct EDA-A1 and X-linked EDA-A2 receptors. We identified a series of novel EDA mutations in families with XLHED, allowing the identification of the following three functionally important regions in EDA: a C-terminal TNF homology domain, a collagen domain, and a furin protease recognition sequence. Mutations in the TNF homology domain impair binding of both splice variants to their receptors. Mutations in the collagen domain can inhibit multimerization of the TNF homology region, whereas those in the consensus furin recognition sequence prevent proteolytic cleavage of EDA. Finally, a mutation affecting an intron splice donor site is predicted to eliminate specifically the EDA-A1 but not the EDA-A2 splice variant. Thus a proteolytically processed, oligomeric form of EDA-A1 is required in vivo for proper morphogenesis.
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The well--known Minkowski's? $(x)$ function is presented as the asymptotic distribution function of an enumeration of the rationals in (0,1] based on their continued fraction representation. Besides, the singularity of ?$(x)$ is clearly proved in two ways: by exhibiting a set of measure one in which ?ï$(x)$ = 0; and again by actually finding a set of measure one which is mapped onto a set of measure zero and viceversa. These sets are described by means of metrical properties of different systems for real number representation.
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Kirje 1.11.1965
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Peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors (RXRs) are nuclear hormone receptors that are activated by fatty acids and 9-cis-retinoic acid, respectively. PPARs and RXRs form heterodimers that activate transcription by binding to PPAR response elements (PPREs) in the promoter of target genes. The PPREs described thus far consist of a direct tandem repeat of the AGGTCA core element with one intervening nucleotide. We show here that the vitellogenin A2 estrogen response element (ERE) can also function as a PPRE and is bound by a PPAR/RXR heterodimer. Although this heterodimer can bind to several other ERE-related palindromic response elements containing AGGTCA half-sites, only the ERE is able to confer transactivation of test reporter plasmids, when the ERE is placed either close to or at a distance from the transcription initiation site. Examination of natural ERE-containing promoters, including the pS2, very-low-density apolipoprotein II and vitellogenin A2 genes, revealed considerable differences in the binding of PPAR/RXR heterodimers to these EREs. In their natural promoter context, these EREs did not allow transcriptional activation by PPARs/RXRs. Analysis of this lack of stimulation of the vitellogenin A2 promoter demonstrated that PPARs/RXRs bind to the ERE but cannot transactivate due to a nonpermissive promoter structure. As a consequence, PPARs/RXRs inhibit transactivation by the estrogen receptor through competition for ERE binding. This is the first example of signaling cross-talk between PPAR/RXR and estrogen receptor.
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Engineering of fetal tissue has a high potential for the treatment of acute and chronic wounds of the skin in humans as these cells have high expansion capacity under simple culture conditions and one organ donation can produce Master Cell Banks which can fabricate over 900 million biological bandages (9 x 12cm). In a Phase 1 clinical safety study, cases are presented for the treatment of therapy resistant leg ulcers. All eight patients, representing 13 ulcers, tolerated multiple treatments with fetal biological bandages showing no negative secondary effects and repair processes similar to that seen in 3rd degree burns. Differential gene profiling using Affymetrix gene chips (analyzing 12,500 genes) were accomplished on these banked fetal dermal skin cells compared to banked dermal skin cells of an aged donor in order to point to potential indicators of wound healing. Families of genes involved in cell adhesion and extracellular matrix, cell cycle, cellular signaling, development and immune response show significant differences in regulation between banked fetal and those from banked old skin cells: with approximately 47.0% of genes over-expressed in fetal fibroblasts. It is perhaps these differences which contribute to efficient tissue repair seen in the clinic with fetal cell therapy.
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Échelle(s) : [ca 1:12 500]
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[Acte royal. 1830-06-13]
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Échelle(s) : [ca 1:9 500] échelle de mille mètres, 1000 Mètres [= 10,5 cm]
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Échelle(s) : [ca 1:175 500], échelle de 20000 mètres [= 11,4 cm]