916 resultados para 1086
Resumo:
While sound and video may capture viewers' attention, interaction can captivate them. This has not been available prior to the advent of Digital Television. In fact, what lies at the heart of the Digital Television revolution is this new type of interactive content, offered in the form of interactive Television (iTV) services. On top of that, the new world of converged networks has created a demand for a new type of converged services on a range of mobile terminals (Tablet PCs, PDAs and mobile phones). This paper aims at presenting a new approach to service creation that allows for the semi-automatic translation of simulations and rapid prototypes created in the accessible desktop multimedia authoring package Macromedia Director into services ready for broadcast. This is achieved by a series of tools that de-skill and speed-up the process of creating digital TV user interfaces (UI) and applications for mobile terminals. The benefits of rapid prototyping are essential for the production of these new types of services, and are therefore discussed in the first section of this paper. In the following sections, an overview of the operation of content, service, creation and management sub-systems is presented, which illustrates why these tools compose an important and integral part of a system responsible of creating, delivering and managing converged broadcast and telecommunications services. The next section examines a number of metadata languages candidates for describing the iTV services user interface and the schema language adopted in this project. A detailed description of the operation of the two tools is provided to offer an insight of how they can be used to de-skill and speed-up the process of creating digital TV user interfaces and applications for mobile terminals. Finally, representative broadcast oriented and telecommunication oriented converged service components are also introduced, demonstrating how these tools have been used to generate different types of services.
Resumo:
This study aimed to evaluate the effect of an e-learning program on the validity and reproducibility of the International Caries Detection and Assessment System (ICDAS) in detecting occlusal caries. For the study, 170 permanent molars were selected. Four dentists in Switzerland who had no previous contact with ICDAS examined the teeth before and after the e-learning program and scored the sites according to ICDAS. Teeth were histologically prepared and assessed for caries extension. The significance level was set at 0.05. Sensitivity before and after the e-learning program was 0.80 and 0.77 (D1), 0.72 and 0.63 (D2), and 0.74 and 0.67 (D3,4), respectively. Specificity was 0.64 and 0.69 (D1), 0.70 and 0.81 (D2), and 0.81 and 0.87 (D3,4). A McNemar test did not show any difference between the values of sensitivity, specificity, accuracy, and area under the ROC curve (AUC) before and after the e-learning program. The averages of wK values for interexaminer reproducibility were 0.61 (before) and 0.66 (after). Correlation with histology presented wK values of 0.62 (before) and 0.63 (after). A Wilcoxon test showed a statistically significant difference between before and after the e-learning program. In conclusion, even though ICDAS performed well in detecting occlusal caries, the e-learning program did not have any statistically significant effect on its performance by these experienced dentists.
Resumo:
P450 oxidoreductase (POR) is the obligatory flavoprotein intermediate that transfers electrons from reduced nicotinamide adenine dinucleotide phosphate (NADPH) to all microsomal cytochrome P450 enzymes. Although mouse Por gene ablation causes embryonic lethality, POR missense mutations cause disordered steroidogenesis, ambiguous genitalia, and Antley-Bixler syndrome (ABS), which has also been attributed to fibroblast growth factor receptor 2 (FGFR2) mutations. We sequenced the POR gene and FGFR2 exons 8 and 10 in 32 individuals with ABS and/or hormonal findings that suggested POR deficiency. POR and FGFR2 mutations segregated completely. Fifteen patients carried POR mutations on both alleles, 4 carried mutations on only one allele, 10 carried FGFR2 or FGFR3 mutations, and 3 patients carried no mutations. The 34 affected POR alleles included 10 with A287P (all from whites) and 7 with R457H (four Japanese, one African, two whites); 17 of the 34 alleles carried 16 "private" mutations, including 9 missense and 7 frameshift mutations. These 11 missense mutations, plus 10 others found in databases or reported elsewhere, were recreated by site-directed mutagenesis and were assessed by four assays: reduction of cytochrome c, oxidation of NADPH, support of 17alpha-hydroxylase activity, and support of 17,20 lyase using human P450c17. Assays that were based on cytochrome c, which is not a physiologic substrate for POR, correlated poorly with clinical phenotype, but assays that were based on POR's support of catalysis by P450c17--the enzyme most closely associated with the hormonal phenotype--provided an excellent genotype/phenotype correlation. Our large survey of patients with ABS shows that individuals with an ABS-like phenotype and normal steroidogenesis have FGFR mutations, whereas those with ambiguous genitalia and disordered steroidogenesis should be recognized as having a distinct new disease: POR deficiency.
Resumo:
INTRODUCTION Transplacental feto-maternal lipid exchange through the ATP-binding cassette transporters ABCA1 and ABCG1 is important for normal fetal development. However, only scarce and conflicting data exist on the involvement of these transporters in gestational disease. METHODS Placenta samples (n = 72) derived from common gestational diseases, including pre-eclampsia (PE), HELLP, intrauterine growth restriction (IUGR), intrahepatic cholestasis of pregnancy and gestational diabetes, were assessed for their ABCA1 and ABCG1 expression levels and compared to age-matched control placentas with qRT-PCR and immunohistochemistry. ABCA1 expression was additionally investigated with immunoblot in placental membrane vesicles. Furthermore, placental cholesterol and phospholipid contents were assessed. RESULTS ABCA1 mRNA levels differed significantly between preterm and term control placentas (p = 0.0013). They were down-regulated in isolated PE and PE with IUGR (p = 0.0006 and p = 0.0012, respectively), but unchanged in isolated IUGR, isolated HELLP and other gestational diseases compared to gestational age-matched controls. Correspondingly, in PE, ABCA1 protein expression was significantly reduced in the apical membrane of the villous syncytiotrophoblast (p = 0.011) and in villous fetal endothelial cells (p = 0.036). Furthermore, in PE there was a significant increase in the placental content of total and individual classes of phospholipids which were partially correlated with diminished ABCA1 expression. Conversely, ABCG1 mRNA and protein levels were stable in the investigated conditions. CONCLUSIONS In gestational disease, there is a specific down-regulation of placental ABCA1 expression at sites of feto-maternal lipid exchange in PE. At a functional level, the increase in placental lipid concentrations provides indirect evidence of an impaired transport capacity of ABCA1 in this disease.