891 resultados para Switch allocation


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The IEEE 802.15.4 standard provides appealing features to simultaneously support real-time and non realtime traffic, but it is only capable of supporting real-time communications from at most seven devices. Additionally, it cannot guarantee delay bounds lower than the superframe duration. Motivated by this problem, in this paper we propose an Explicit Guaranteed time slot Sharing and Allocation scheme (EGSA) for beacon-enabled IEEE 802.15.4 networks. This scheme is capable of providing tighter delay bounds for real-time communications by splitting the Contention Free access Period (CFP) into smaller mini time slots and by means of a new guaranteed bandwidth allocation scheme for a set of devices with periodic messages. At the same the novel bandwidth allocation scheme can maximize the duration of the CFP for non real-time communications. Performance analysis results show that the EGSA scheme works efficiently and outperforms competitor schemes both in terms of guaranteed delay and bandwidth utilization.

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We present an algorithm for bandwidth allocation for delay-sensitive traffic in multi-hop wireless sensor networks. Our solution considers both periodic as well as aperiodic real-time traffic in an unified manner. We also present a distributed MAC protocol that conforms to the bandwidth allocation and thus satisfies the latency requirements of realtime traffic. Additionally, the protocol provides best-effort service to non real-time traffic. We derive the utilization bounds of our MAC protocol.

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The IEEE 802.15.4 protocol proposes a flexible communication solution for Low-Rate Wireless Personal Area Networks including sensor networks. It presents the advantage to fit different requirements of potential applications by adequately setting its parameters. When enabling its beacon mode, the protocol makes possible real-time guarantees by using its Guaranteed Time Slot (GTS) mechanism. This paper analyzes the performance of the GTS allocation mechanism in IEEE 802.15.4. The analysis gives a full understanding of the behavior of the GTS mechanism with regards to delay and throughput metrics. First, we propose two accurate models of service curves for a GTS allocation as a function of the IEEE 802.15.4 parameters. We then evaluate the delay bounds guaranteed by an allocation of a GTS using Network Calculus formalism. Finally, based on the analytic results, we analyze the impact of the IEEE 802.15.4 parameters on the throughput and delay bound guaranteed by a GTS allocation. The results of this work pave the way for an efficient dimensioning of an IEEE 802.15.4 cluster.

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The IEEE 802.15.4 protocol proposes a flexible communication solution for Low-Rate Wireless Personal Area Networks (LR-WPAN) including wireless sensor networks (WSNs). It presents the advantage to fit different requirements of potential applications by adequately setting its parameters. When in beaconenabled mode, the protocol can provide timeliness guarantees by using its Guaranteed Time Slot (GTS) mechanism. However, power-efficiency and timeliness guarantees are often two antagonistic requirements in wireless sensor networks. The purpose of this paper is to analyze and propose a methodology for setting the relevant parameters of IEEE 802.15.4-compliant WSNs that takes into account a proper trade-off between power-efficiency and delay bound guarantees. First, we propose two accurate models of service curves for a GTS allocation as a function of the IEEE 802.15.4 parameters, using Network Calculus formalism. We then evaluate the delay bound guaranteed by a GTS allocation and express it as a function of the duty cycle. Based on the relation between the delay requirement and the duty cycle, we propose a power-efficient superframe selection method that simultaneously reduces power consumption and enables meeting the delay requirements of real-time flows allocating GTSs. The results of this work may pave the way for a powerefficient management of the GTS mechanism in an IEEE 802.15.4 cluster.

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The high penetration of distributed energy resources (DER) in distribution networks and the competitiveenvironment of electricity markets impose the use of new approaches in several domains. The networkcost allocation, traditionally used in transmission networks, should be adapted and used in the distribu-tion networks considering the specifications of the connected resources. The main goal is to develop afairer methodology trying to distribute the distribution network use costs to all players which are usingthe network in each period. In this paper, a model considering different type of costs (fixed, losses, andcongestion costs) is proposed comprising the use of a large set of DER, namely distributed generation(DG), demand response (DR) of direct load control type, energy storage systems (ESS), and electric vehi-cles with capability of discharging energy to the network, which is known as vehicle-to-grid (V2G). Theproposed model includes three distinct phases of operation. The first phase of the model consists in aneconomic dispatch based on an AC optimal power flow (AC-OPF); in the second phase Kirschen’s andBialek’s tracing algorithms are used and compared to evaluate the impact of each resource in the net-work. Finally, the MW-mile method is used in the third phase of the proposed model. A distributionnetwork of 33 buses with large penetration of DER is used to illustrate the application of the proposedmodel.

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Dispersion of returns has gained a lot of attention as a measure to distinguish good and bad investment opportunities time. In the following dissertation, the cross-sectional returns volatility is analyzed over a fifteen year period across the S&P100 Index composition. The main inference drawn from the data sample is that the canonical measure of dispersion is highly macro-risk driven and therefore more biased towards returns volatility rather than its correlation component.

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Rubisco is responsible for the fixation of CO2 into organic compounds through photosynthesis and thus has a great agronomic importance. It is well established that this enzyme suffers from a slow catalysis, and its low specificity results into photorespiration, which is considered as an energy waste for the plant. However, natural variations exist, and some Rubisco lineages, such as in C4 plants, exhibit higher catalytic efficiencies coupled to lower specificities. These C4 kinetics could have evolved as an adaptation to the higher CO2 concentration present in C4 photosynthetic cells. In this study, using phylogenetic analyses on a large data set of C3 and C4 monocots, we showed that the rbcL gene, which encodes the large subunit of Rubisco, evolved under positive selection in independent C4 lineages. This confirms that selective pressures on Rubisco have been switched in C4 plants by the high CO2 environment prevailing in their photosynthetic cells. Eight rbcL codons evolving under positive selection in C4 clades were involved in parallel changes among the 23 independent monocot C4 lineages included in this study. These amino acids are potentially responsible for the C4 kinetics, and their identification opens new roads for human-directed Rubisco engineering. The introgression of C4-like high-efficiency Rubisco would strongly enhance C3 crop yields in the future CO2-enriched atmosphere.

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Peroxisome proliferator-activated receptors (PPARs) compose a family of nuclear receptors that mediate the effects of lipidic ligands at the transcriptional level. In this review, we highlight advances in the understanding of the PPAR ligand binding domain (LBD) structure at the atomic level. The overall structure of PPARs LBD is described, and important protein ligand interactions are presented. Structure-activity relationships between isotypes structures and ligand specificity are addressed. It is shown that the numerous experimental three-dimensional structures available, together with in silico simulations, help understanding the role played by the activating function-2 (AF-2) in PPARs activation and its underlying molecular mechanism. The relation between the PPARs constitutive activity and the intrinsic stability of the active conformation is discussed. Finally, the interactions of PPARs LBD with co-activators or co-repressors, as well as with the retinoid X receptor (RXR) are described and considered in relation to PPARs activation.

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Purpose: Sirolimus (SRL) has been used to replace calcineurin inhibitors (CNI) for various indications including CNI-induced toxicity. The aim of this study was to evaluate the efficacy and safety of switching from CNI to SRL in stable renal transplant recipients (RTR) with low grade proteinuria (<1 g/24 h). Methods and materials: Between 2001 and 2007, 41 patients (20 females, 21 males; mean age 47 ± 13) were switched after a median time post-transplantation of 73.5 months (range 0.2-273.2 months). Indications for switch were CNI nephrotoxicity (39%), thrombotic micro-angiopathy (14.6%), post-transplantation cancer (24.4%), CNI neurotoxicity (7.4%), or others (14.6%). Mean follow-up after SRL switch was 23.8±16.3 months. Mean SRL dosage and through levels were 2.4 ± 1.1 mg/day and 8 ± 2.2 ug/l respectively. Immunosuppressive regiments were SRL + mycophenolate mofetil (MMF) (31.7%), SRL + MMF + prednisone (36.58%), SRL + prednisone (19.51%), SRL + Azathioprine (9.75%), or SRL alone (2.43%). Results: Mean creatinine decreased from 164 to 143 μmol/l (p <0.03), mean estimated glomerular filtration rate (eGFR) increased significantly from 50.13 to 55.01 ml/minute (p <0.00001), mean systolic and diastolic blood pressure decreased from 138 to 132 mm Hg (p <0.03) and from 83 to78 mm Hg (p <0.01), but mean proteinuria increased from 0.21 to 0.63 g/24 h (p <0.001). While mean total cholesterolemia didn't increased significantly from 5.09 to 5.56 mmol/l (p = 0.06). The main complications after SRL switch were dermatitis (19.5%), urinary tract infections (24.4%), ankle edema (13.3%), and transient oral ulcers (20%). Acute rejection after the switch occurred in 7.3% of patients (n = 3), and 2 acute rejections were successfully treated with corticosteroids and 1 did not respond to treatment (not related to switch). SRL had to be discontinued in 17% of patients (2 nephrotic syndromes, 2 severe edema, 1 acute rejection, 1 thrombotic micro-angiopathy, and 1 fever). Conclusion: In conclusion, we found that switching from CNI to SRL in stable RTR was safe and associated with a significant improvement of renal function and blood pressure. Known side-effects of SRL led to drug discontinuation in less than 20% of patients and the acute rejection rate was 7.3%. This experience underlines the importance of patient selection before switching to SRL, in particular regarding preswitch proteinuria.

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QUESTION UNDER STUDY: To assess which high-risk acute coronary syndrome (ACS) patient characteristics played a role in prioritising access to intensive care unit (ICU), and whether introducing clinical practice guidelines (CPG) explicitly stating ICU admission criteria altered this practice. PATIENTS AND METHODS: All consecutive patients with ACS admitted to our medical emergency centre over 3 months before and after CPG implementation were prospectively assessed. The impact of demographic and clinical characteristics (age, gender, cardiovascular risk factors, and clinical parameters upon admission) on ICU hospitalisation of high-risk patients (defined as retrosternal pain of prolonged duration with ECG changes and/or positive troponin blood level) was studied by logistic regression. RESULTS: Before and after CPG implementation, 328 and 364 patients, respectively, were assessed for suspicion of ACS. Before CPG implementation, 36 of the 81 high-risk patients (44.4%) were admitted to ICU. After CPG implementation, 35 of the 90 high-risk patients (38.9%) were admitted to ICU. Male patients were more frequently admitted to ICU before CPG implementation (OR=7.45, 95% CI 2.10-26.44), but not after (OR=0.73, 95% CI 0.20-2.66). Age played a significant role in both periods (OR=1.57, 95% CI 1.24-1.99), both young and advanced ages significantly reducing ICU admission, but to a lesser extent after CPG implementation. CONCLUSION: Prioritisation of access to ICU for high-risk ACS patients was age-dependent, but focused on the cardiovascular risk factor profile. CPG implementation explicitly stating ICU admission criteria decreased discrimination against women, but other factors are likely to play a role in bed allocation.

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The final decision on cell fate, survival versus cell death, relies on complex and tightly regulated checkpoint mechanisms. The caspase-3 protease is a predominant player in the execution of apoptosis. However, recent progress has shown that this protease paradoxically can also protect cells from death. Here, we discuss the underappreciated, protective, and prosurvival role of caspase-3 and detail the evidence showing that caspase-3, through differential processing of p120 Ras GTPase-activating protein (RasGAP), can modulate a given set of proteins to generate, depending on the intensity of the input signals, opposite outcomes (survival vs death).

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PPARs (peroxisome-proliferator-activated receptors) alpha, beta/delta and gamma are a group of transcription factors that are involved in numerous processes, including lipid metabolism and adipogenesis. By comparing liver mRNAs of wild-type and PPARalpha-null mice using microarrays, a novel putative target gene of PPARalpha, G0S2 (G0/G1 switch gene 2), was identified. Hepatic expression of G0S2 was up-regulated by fasting and by the PPARalpha agonist Wy14643 in a PPARalpha-dependent manner. Surprisingly, the G0S2 mRNA level was highest in brown and white adipose tissue and was greatly up-regulated during mouse 3T3-L1 and human SGBS (Simpson-Golabi-Behmel syndrome) adipogenesis. Transactivation, gel shift and chromatin immunoprecipitation assays indicated that G0S2 is a direct PPARgamma and probable PPARalpha target gene with a functional PPRE (PPAR-responsive element) in its promoter. Up-regulation of G0S2 mRNA seemed to be specific for adipogenesis, and was not observed during osteogenesis or myogenesis. In 3T3-L1 fibroblasts, expression of G0S2 was associated with growth arrest, which is required for 3T3-L1 adipogenesis. Together, these data indicate that G0S2 is a novel target gene of PPARs that may be involved in adipocyte differentiation.

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A single coronary artery can complicate the surgical technique of arterial switch operations, impairing early and late outcomes. We propose a new surgical approach, successfully applied in a 2.1 kg neonate, aimed at reducing the risk of early and late compression and/or distortion of the newly constructed coronary artery system.

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BACKGROUND: Hyperzincemia and hypercalprotectinemia (Hz/Hc) is a distinct autoinflammatory entity involving extremely high serum concentrations of the proinflammatory alarmin myeloid-related protein (MRP) 8/14 (S100A8/S100A9 and calprotectin). OBJECTIVE: We sought to characterize the genetic cause and clinical spectrum of Hz/Hc. METHODS: Proline-serine-threonine phosphatase-interacting protein 1 (PSTPIP1) gene sequencing was performed in 14 patients with Hz/Hc, and their clinical phenotype was compared with that of 11 patients with pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome. PSTPIP1-pyrin interactions were analyzed by means of immunoprecipitation and Western blotting. A structural model of the PSTPIP1 dimer was generated. Cytokine profiles were analyzed by using the multiplex immunoassay, and MRP8/14 serum concentrations were analyzed by using an ELISA. RESULTS: Thirteen patients were heterozygous for a missense mutation in the PSTPIP1 gene, resulting in a p.E250K mutation, and 1 carried a mutation resulting in p.E257K. Both mutations substantially alter the electrostatic potential of the PSTPIP1 dimer model in a region critical for protein-protein interaction. Patients with Hz/Hc have extremely high MRP8/14 concentrations (2045 ± 1300 μg/mL) compared with those with PAPA syndrome (116 ± 74 μg/mL) and have a distinct clinical phenotype. A specific cytokine profile is associated with Hz/Hc. Hz/Hc mutations altered protein binding of PSTPIP1, increasing interaction with pyrin through phosphorylation of PSTPIP1. CONCLUSION: Mutations resulting in charge reversal in the y-domain of PSTPIP1 (E→K) and increased interaction with pyrin cause a distinct autoinflammatory disorder defined by clinical and biochemical features not found in patients with PAPA syndrome, indicating a unique genotype-phenotype correlation for mutations in the PSTPIP1 gene. This is the first inborn autoinflammatory syndrome in which inflammation is driven by uncontrolled release of members of the alarmin family.