201 research outputs found

    Distributed scheduling based on multi-agent systems and optimization methods

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    The increasing relevance of complex systems in dynamic environments has received special attention during the last decade from the researchers. Such systems need to satisfy products or clients desires, which, after accomplished might change, becoming a very dynamic situation. Currently, decentralized approaches could assist in the automation of dynamic scheduling, based on the distribution of control functions over a swarm network of decision-making entities. Distributed scheduling, in an automatic manner, can be answered by a service coordination architecture of the different schedule components. However, it is necessary to introduce the control layer in the solution, encapsulating an intelligent service that merge agents with optimization methods. Multi-agent systems (MAS) can be combined with several optimization methods to extract the best of the two worlds: the intelligent control, cooperation and autonomy provided by MAS solutions and the optimum offered by optimization methods. The proposal intends to test the intelligent management of the schedule composition quality, in two case studies namely, manufacturing and home health care.FCT - Fundação para a Ciência e a Tecnologia (UID/CEC/00319/2019

    Guidelines for the deployment and implementation of manufacturing scheduling systems

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    It has frequently been stated that there exists a gap between production scheduling theory and practice. In order to put theoretical findings into practice, advances in scheduling models and solution procedures should be embedded into a piece of software - a scheduling system - in companies. This results in a process that entails (1) determining its functional features, and (2) adopting a successful strategy for its development and deployment. In this paper we address the latter question and review the related literature in order to identify descriptions and recommendations of the main aspects to be taken into account when developing such systems. These issues are then discussed and classified, resulting in a set of guidelines that can help practitioners during the process of developing and deploying a scheduling system. In addition, identification of these issues can provide some insights to drive theoretical scheduling research towards those topics more in demand by practitioners, and thus help to close the aforementioned gap.Framiñan Torres, JM.; Ruiz García, R. (2012). Guidelines for the deployment and implementation of manufacturing scheduling systems. International Journal of Production Research. 50(7):1799-1812. doi:10.1080/00207543.2011.564670S17991812507Baek, D. H. (1999). A visualized human-computer interactive approach to job shop scheduling. International Journal of Computer Integrated Manufacturing, 12(1), 75-83. doi:10.1080/095119299130489Comesaña Benavides, J. A., & Carlos Prado, J. (2002). Creating an expert system for detailed scheduling. International Journal of Operations & Production Management, 22(7), 806-819. doi:10.1108/01443570210433562Bensana, E. 1986. An expert-system approach to industrial job-shop scheduling. 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    Is Tail-Optimal Scheduling Possible?

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    A Tight 2-Approximation for Preemptive Stochastic Scheduling

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    Endoplasmic reticulum stress signalling – from basic mechanisms to clinical applications

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    The endoplasmic reticulum (ER) is a membranous intracellular organelle and the first compartment of the secretory pathway. As such, the ER contributes to the production and folding of approximately one‐third of cellular proteins, and is thus inextricably linked to the maintenance of cellular homeostasis and the fine balance between health and disease. Specific ER stress signalling pathways, collectively known as the unfolded protein response (UPR), are required for maintaining ER homeostasis. The UPR is triggered when ER protein folding capacity is overwhelmed by cellular demand and the UPR initially aims to restore ER homeostasis and normal cellular functions. However, if this fails, then the UPR triggers cell death. In this review, we provide a UPR signalling‐centric view of ER functions, from the ER's discovery to the latest advancements in the understanding of ER and UPR biology. Our review provides a synthesis of intracellular ER signalling revolving around proteostasis and the UPR, its impact on other organelles and cellular behaviour, its multifaceted and dynamic response to stress and its role in physiology, before finally exploring the potential exploitation of this knowledge to tackle unresolved biological questions and address unmet biomedical needs. Thus, we provide an integrated and global view of existing literature on ER signalling pathways and their use for therapeutic purposes

    Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

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    Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

    Gene therapy for carcinoma of the breast: Genetic toxins

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    Gene therapy was initially envisaged as a potential treatment for genetically inherited, monogenic disorders. The applications of gene therapy have now become wider, however, and include cardiovascular diseases, vaccination and cancers in which conventional therapies have failed. With regard to oncology, various gene therapy approaches have been developed. Among them, the use of genetic toxins to kill cancer cells selectively is emerging. Two different types of genetic toxins have been developed so far: the metabolic toxins and the dominant-negative class of toxins. This review describes these two different approaches, and discusses their potential applications in cancer gene therapy
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