Automated Network Service Scaling in NFV: Concepts, Mechanisms and Scaling Workflow

Next-generation systems are anticipated to be digital platforms supporting innovative services with rapidly changing traffic patterns. To cope with this dynamicity in a cost-efficient manner, operators need advanced service management capabilities such as those provided by NFV. NFV enables operators to scale network services with higher granularity and agility than today. For this end, automation is key. In search of this automation, the European Telecommunications Standards Institute (ETSI) has defined a reference NFV framework that make use of model-driven templates called Network Service Descriptors (NSDs) to operate network services through their lifecycle. For the scaling operation, an NSD defines a discrete set of instantiation levels among which a network service instance can be resized throughout its lifecycle. Thus, the design of these levels is key for ensuring an effective scaling. In this article, we provide an overview of the automation of the network service scaling operation in NFV, addressing the options and boundaries introduced by ETSI normative specifications. We start by providing a description of the NSD structure, focusing on how instantiation levels are constructed. For illustrative purposes, we propose an NSD for a representative NS. This NSD includes different instantiation levels that enable different ways to automatically scale this NS. Then, we show the different scaling procedures the NFV framework has available, and how it may automate their triggering. Finally, we propose an ETSI-compliant workflow to describe in detail a representative scaling procedure. This workflow clarifies the interactions and information exchanges between the functional blocks in the NFV framework when performing the scaling operation.Comment: This work has been accepted for publication in the IEEE Communications Magazin

Reforço do sistema de revestimento da cobertura do Pavilhão Multiusos de Baião

O pavilhão Multiusos de Baião foi construído em 2004. O edifício é formado essen-cialmente por dois corpos. A cobertura do corpo de maior dimensão é de uma água, cuja estru-tura principal, em madeira lamelada colada, é constituída por vigas treliçadas do tipo barriga de peixe, madres de cobertura e elementos de contraventamento. Com a ocorrência de ventos fortes observaram-se levantamentos do revestimento da cobertura em duas zonas do pavilhão. Neste artigo é descrito o resultado do trabalho de análise da referida patologia, as suas causas, e é apresentada a solução de reforço proposta para o sistema de fixação do revestimento da cobertura, com recurso a ligadores metálicos

A Nanostructured Piezoelectric Immunosensor for Detection of Human Cardiac Troponin T

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)A piezoelectric immunosensor based on gold nanoparticles (AuNPs) co-immobilized on a dithiol-modified surface is proposed for detection of human cardiac troponin T (TnT). Anti-human troponin T (anti-TnT) antibodies were covalently immobilized on the nanostructured electrode surface by thiol-aldehyde linkages. In a homogeneous bulk solution, TnT was captured by anti-TnT immobilized on the QCM electrode. Cyclic voltammetry studies were used to characterize the AuNPs layer on the electrode surface and the anti-TnT immobilization steps. The QCM-flow immunosensor exhibited good reliability, measuring concentrations of TnT from 0.003 to 0.5 ng mL(-1) in human serum with high linearity (r = 0.989; p < 0.01). The immunosensor exhibited a 7% coefficient of variation and 0.0015 ng mL(-1) limit of detection, indicating a high reproducibility and sensitivity. The proposed QCM nanostructured immunosensor is easy to use and has promising potential in the diagnosis of acute myocardial infarction due to its speed and high sensitivity.11111078510797Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)CNPq [483242/2010-1

Integration of PV Distributed Generators into Electrical Networks for Investment and Energy Purchase Costs Reduction by Using a Discrete–Continuous Parallel PSO

The problem of optimally integrating PV DGs into electrical networks to reduce annual costs (which include energy purchase and investment costs) was addressed in this research by presenting a new solution methodology. For such purpose, we used a Discrete–Continuous Parallel Particle Swarm Optimization method (DCPPSO), which considers both the discrete and continuous variables associated with the location and sizing of DGs in an electrical network and employs a parallel processing tool to reduce processing times. The optimization parameters of the proposed solution methodology were tuned using an external optimization algorithm. To validate the performance of DCPPSO, we employed the 33- and 69-bus test systems and compared it with five other solution methods: the BONMIN solver of the General Algebraic Modeling System (GAMS) and other four discrete–continuous methodologies that have been recently proposed. According to the findings, the DCPPSO produced the best results in terms of quality of the solution, processing time, and repeatability in electrical networks of any size, since it showed a better performance as the size of the electrical system increased. © 2022 by the authors

Programa de melhoramento de bananeira no Brasil - resultados recentes.

Principais cultivares. Etapas do Programa de Melhoramento. Resultados obtidos nos últimos três anos. Avaliação para resistência ao desprendimento de fruto. Avaliação para resistência a doenças. Diplóides. Tetraplóides / triplóides. Avaliação de variedades / Híbridos. Pós-colheita. Cultivares recomendadas. Seleção de clones cavendish. Mutação. Propostas futuras. Distribuição de mudas.bitstream/item/112872/1/doc-123.pd

Morphine activates neuroinflammation in a manner parallel to endotoxin

Opioids create a neuroinflammatory response within the CNS, compromising opioid-induced analgesia and contributing to various unwanted actions. How this occurs is unknown but has been assumed to be via classic opioid receptors. Herein, we provide direct evidence that morphine creates neuroinflammation via the activation of an innate immune receptor and not via classic opioid receptors. We demonstrate that morphine binds to an accessory protein of Toll-like receptor 4 (TLR4), myeloid differentiation protein 2 (MD-2), thereby inducing TLR4 oligomerization and triggering proinflammation. Small-molecule inhibitors, RNA interference, and genetic knockout validate the TLR4/MD-2 complex as a feasible target for beneficially modifying morphine actions. Disrupting TLR4/MD-2 protein–protein association potentiated morphine analgesia in vivo and abolished morphine-induced proinflammation in vitro, the latter demonstrating that morphine-induced proinflammation only depends on TLR4, despite the presence of opioid receptors. These results provide an exciting, nonconventional avenue to improving the clinical efficacy of opioids.Xiaohui Wang, Lisa C. Loram, Khara Ramos, Armando J. de Jesus, Jacob Thomas, Kui Cheng, Anireddy Reddy, Andrew A. Somogyi, Mark R. Hutchinson, Linda R. Watkins and Hang Yi

A factorial design for optimization of the analytical variables on the development of a genoassay for the transgenic soybean detection

At the laboratory, analytical method optimizations are performed to achieve the maximum sensitivity and selectivity. Routinely, this procedure is carried out by optimizing one-factor-at-a-time approach until there is no further improvement, where each experimental parameter is optimized separately and independently of the other factors.N/

Loss of SRSF3 in Cardiomyocytes Leads to Decapping of Contraction-Related mRNAs and Severe Systolic Dysfunction

RATIONALE: RBPs (RNA binding proteins) play critical roles in the cell by regulating mRNA transport, splicing, editing, and stability. The RBP SRSF3 (serine/arginine-rich splicing factor 3) is essential for blastocyst formation and for proper liver development and function. However, its role in the heart has not been explored. OBJECTIVE: To investigate the role of SRSF3 in cardiac function. METHODS AND RESULTS: Cardiac SRSF3 expression was high at mid gestation and decreased during late embryonic development. Mice lacking SRSF3 in the embryonic heart showed impaired cardiomyocyte proliferation and died in utero. In the adult heart, SRSF3 expression was reduced after myocardial infarction, suggesting a possible role in cardiac homeostasis. To determine the role of this RBP in the adult heart, we used an inducible, cardiomyocyte-specific SRSF3 knockout mouse model. After SRSF3 depletion in cardiomyocytes, mice developed severe systolic dysfunction that resulted in death within 8 days. RNA-Seq analysis revealed downregulation of mRNAs encoding sarcomeric and calcium handling proteins. Cardiomyocyte-specific SRSF3 knockout mice also showed evidence of alternative splicing of mTOR (mammalian target of rapamycin) mRNA, generating a shorter protein isoform lacking catalytic activity. This was associated with decreased phosphorylation of 4E-BP1 (eIF4E-binding protein 1), a protein that binds to eIF4E (eukaryotic translation initiation factor 4E) and prevents mRNA decapping. Consequently, we found increased decapping of mRNAs encoding proteins involved in cardiac contraction. Decapping was partially reversed by mTOR activation. CONCLUSIONS: We show that cardiomyocyte-specific loss of SRSF3 expression results in decapping of critical mRNAs involved in cardiac contraction. The molecular mechanism underlying this effect likely involves the generation of a short mTOR isoform by alternative splicing, resulting in reduced 4E-BP1 phosphorylation. The identification of mRNA decapping as a mechanism of systolic heart failure may open the way to the development of urgently needed therapeutic tools.This study was supported by grants from the European Union (CardioNeT-ITN-289600 and CardioNext-ITN-608027 to E.L-P.), from the Spanish Ministerio de Economía y Competitividad (RTI2018-096961-BI00, SAF2015-65722-R and SAF2012-31451 to E.L-P.; BIO2015-67580-P and PGC2018-097019-B-I00 to J.V.), the Spanish Carlos III Institute of Health (CPII14/00027 to E.L-P, RD12/0042/066 to P.G.-P. and E.L-P, and RD12/0042/0056, PRB2-IPT13/0001-ISCIII-SGEFI/FEDER, ProteoRed to J.V.), the Madrid Regional Government (2010-BMD-2321 “Fibroteam” to E.L-P.). This study was also supported by the Plan Estatal de I+D+I 2013-2016 – European Regional Development Fund (ERDF) “A way of making Europe”, Spain. The CNIC is supported by the Ministerio de Ciencia, Innovación y Universidades (MCNU) and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505).S