6 resultados para ILLUSTRATED KEY

em Instituto Politécnico do Porto, Portugal


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This paper presents a biased random-key genetic algorithm for the resource constrained project scheduling problem. The chromosome representation of the problem is based on random keys. Active schedules are constructed using a priority-rule heuristic in which the priorities of the activities are defined by the genetic algorithm. A forward-backward improvement procedure is applied to all solutions. The chromosomes supplied by the genetic algorithm are adjusted to reflect the solutions obtained by the improvement procedure. The heuristic is tested on a set of standard problems taken from the literature and compared with other approaches. The computational results validate the effectiveness of the proposed algorithm.

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This paper presents a genetic algorithm for the Resource Constrained Project Scheduling Problem (RCPSP). The chromosome representation of the problem is based on random keys. The schedule is constructed using a heuristic priority rule in which the priorities of the activities are defined by the genetic algorithm. The heuristic generates parameterized active schedules. The approach was tested on a set of standard problems taken from the literature and compared with other approaches. The computational results validate the effectiveness of the proposed algorithm.

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This essay offers a reflection on the concepts of identity and personal narrative, a line of argument that is closely interlaced with a subject‘s capacity to self-representation. As self-representation is necessarily composed upon remembrance processes, the question of memory as an element that directly influences the formation of an individual‘s identity becomes an emergent topic. Bearing this objective in mind, I shall highlight the notion of biographic continuity, the ability to elaborate a personal narrative, as an essential prerogative to attain a sense of identitary cohesion and coherence. On the other hand, I will argue that not only experienced memories play a key role in this process; intermediated, received narratives from the past, memories transmitted either symbolically or by elder members of the group or, what has been meanwhile termed ―postmemory‖, also influence the development of an individual‘s identitary map. This theoretical framework will be illustrated with the novel Paul Schatz im Uhrenkasten, written by German post-Holocaust author Jan Koneffke.

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This essay analyses how the different types of memory may influence the process of identity formation. It shall be argued that not only memories formed upon the subject’s experiences play a key role in this process; intermediated, received narratives from the past, memories transmitted either symbolically or by elder members of the group, or, what has been meanwhile termed as “postmemory”, also play an important part in the development of an individual’s identitary map. This theoretical framework will be illustrated with the novelistic work of Austrian Israeli-born historian, writer and political activist Doron Rabinovici (*1961). As a representative of the so-called “second generation” of Holocaust writers, a generation of individuals who did not experience the nazi genocide violence, but who had to form their identities under the shadow of such a brutal past, Rabinovici addresses essential topics such as the intergenerational transmission of memory and guilt within survivor families, identity formation of second generation individuals (Jews and non-Jews) and the question of simultaneously belonging to different social, historical and linguistic contexts.

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The change of paradigm imposed by the Bologna process, in which the student will be responsible for their own learning, and the presence of a new generation of students with higher technological skills, represent a huge challenge for higher education institutions. The use of new Web Social concepts in teaching process, supported by applications commonly called Web 2.0, with which these new students feel at ease, can bring benefits in terms of motivation and the frequency and quality of students' involvement in academic activities. An e-learning platform with web-based applications as a complement can significantly contribute to the development of different skills in higher education students, covering areas which are usually in deficit.

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Transthyretin (TTR) protects against A-Beta toxicity by binding the peptide thus inhibiting its aggregation. Previous work showed different TTR mutations interact differently with A-Beta, with increasing affinities correlating with decreasing amyloidogenecity of the TTR mutant; this did not impact on the levels of inhibition of A-Beta aggregation, as assessed by transmission electron microscopy. Our work aimed at probing differences in binding to A-Beta by WT, T119M and L55P TTR using quantitative assays, and at identifying factors affecting this interaction. We addressed the impact of such factors in TTR ability to degrade A-Beta. Using a dot blot approach with the anti-oligomeric antibody A11, we showed that A-Beta formed oligomers transiently, indicating aggregation and fibril formation, whereas in the presence of WT and T119M TTR the oligomers persisted longer, indicative that these variants avoided further aggregation into fibrils. In contrast, L55PTTR was not able to inhibit oligomerization or to prevent evolution to aggregates and fibrils. Furthermore, apoptosis assessment showed WT and T119M TTR were able to protect against A-Beta toxicity. Because the amyloidogenic potential of TTR is inversely correlated with its stability, the use of drugs able to stabilize TTR tetrameric fold could result in increased TTR/ABeta binding. Here we showed that iododiflunisal, 3-dinitrophenol, resveratrol, [2-(3,5-dichlorophenyl)amino] (DCPA) and [4- (3,5-difluorophenyl)] (DFPB) were able to increase TTR binding to A-Beta; however only DCPA and DFPB improved TTR proteolytic activity. Thyroxine, a TTR ligand, did not influence TTR/A-Beta interaction and A-Beta degradation by TTR, whereas RBP, another TTR ligand, not only obstructed the interaction but also inhibited TTR proteolytic activity. Our results showed differences between WT and T119M TTR, and L55PTTR mutant regarding their interaction with A-Beta and prompt the stability of TTR as a key factor in this interaction, which may be relevant in AD pathogenesis and for the design of therapeutic TTR-based therapies.