959 resultados para cascade of pi-circuits


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[EN]Facial image processing is becoming widespread in human-computer applications, despite its complexity. High-level processes such as face recognition or gender determination rely on low-level routines that must e ectively detect and normalize the faces that appear in the input image. In this paper, a face detection and normalization system is described. The approach taken is based on a cascade of fast, weak classi ers that together try to determine whether a frontal face is present in the image.

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During their life cycle, plants are typically confronted by simultaneous biotic and abiotic stresses. Low inorganic phosphate (Pi) is one of the most common nutrient deficiencies limiting plant growth in natural and agricultural ecosystems, while insect herbivory accounts for major losses in plant productivity and impacts ecological and evolutionary changes in plant populations. Here, we report that plants experiencing Pi deficiency induce the jasmonic acid (JA) pathway and enhance their defense against insect herbivory. Pi-deficient Arabidopsis (Arabidopsis thaliana) showed enhanced synthesis of JA and the bioactive conjugate JA-isoleucine, as well as activation of the JA signaling pathway, in both shoots and roots of wild-type plants and in shoots of the Pi-deficient mutant pho1 The kinetics of the induction of the JA signaling pathway by Pi deficiency was influenced by PHOSPHATE STARVATION RESPONSE1, the main transcription factor regulating the expression of Pi starvation-induced genes. Phenotypes of the pho1 mutant typically associated with Pi deficiency, such as high shoot anthocyanin levels and poor shoot growth, were significantly attenuated by blocking the JA biosynthesis or signaling pathway. Wounded pho1 leaves hyperaccumulated JA/JA-isoleucine in comparison with the wild type. The pho1 mutant also showed an increased resistance against the generalist herbivore Spodoptera littoralis that was attenuated in JA biosynthesis and signaling mutants. Pi deficiency also triggered increased resistance to S. littoralis in wild-type Arabidopsis as well as tomato (Solanum lycopersicum) and Nicotiana benthamiana, revealing that the link between Pi deficiency and enhanced herbivory resistance is conserved in a diversity of plants, including crops.

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Thesis (Ph.D.)--University of Washington, 2016-08

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Thesis (Ph.D.)--University of Washington, 2016-06

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Résumé : Le transistor monoélectronique (SET) est un dispositif nanoélectronique très attractif à cause de son ultra-basse consommation d’énergie et sa forte densité d’intégration, mais il n’a pas les capacités suffisantes pour pouvoir remplacer complètement la technologie CMOS. Cependant, la combinaison de la technologie SET avec celle du CMOS est une voie intéressante puisqu’elle permet de profiter des forces de chacune, afin d’obtenir des circuits avec des fonctionnalités additionnelles et uniques. Cette thèse porte sur l’intégration 3D monolithique de nanodispositifs dans le back-end-of-line (BEOL) d’une puce CMOS. Cette approche permet d’obtenir des circuits hybrides et de donner une valeur ajoutée aux puces CMOS actuelles sans altérer le procédé de fabrication du niveau des transistors MOS. L’étude se base sur le procédé nanodamascène classique développé à l’UdeS qui a permis la fabrication de dispositifs nanoélectroniques sur un substrat de SiO2. Ce document présente les travaux réalisés sur l’optimisation du procédé de fabrication nanodamascène, afin de le rendre compatible avec le BEOL de circuits CMOS. Des procédés de gravure plasma adaptés à la fabrication de nanostructures métalliques et diélectriques sont ainsi développés. Le nouveau procédé nanodamascène inverse a permis de fabriquer des jonctions MIM et des SET métalliques sur une couche de SiO2. Les caractérisations électriques de MIM et de SET formés avec des jonctions TiN/Al2O3 ont permis de démontrer la présence de pièges dans les jonctions et la fonctionnalité d’un SET à basse température (1,5 K). Le transfert de ce procédé sur CMOS et le procédé d’interconnexions verticales sont aussi développés par la suite. Finalement, un circuit 3D composé d’un nanofil de titane connecté verticalement à un transistor MOS est réalisé et caractérisé avec succès. Les résultats obtenus lors de cette thèse permettent de valider la possibilité de co-intégrer verticalement des dispositifs nanoélectroniques avec une technologie CMOS, en utilisant un procédé de fabrication compatible.

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Räjähdysvaaralliset tilat aiheuttavat lisävaatimuksia instrumentointisuunnittelulle. Tämän diplomityön tavoitteena on kartoittaa räjähdysvaarallisten tilojen standardien vaatimuksia instrumentoinnin suunnitteluun ja laitevalintoihin. Tarkemmin tarkastellaan luonnostaan vaaratonta räjähdyssuojausrakennetta, joita instrumentoinnin laitteilla tyypillisesti käytetään. Luonnostaan vaarattomassa räjähdyssuojausrakenteessa sähkölaitteen energiaa ja pintalämpötilaa rajoitetaan niin, ettei laite voi sytyttää räjähdysvaarallista seosta. Työssä perehdytään myös luonnostaan vaarattomia laitteita sisältäviin instrumentointipiireihin ja standardin niille asettamiin vaatimuksiin. Tällaisille piireille on tehtävä varmennustarkastelu, jossa todennetaan piirin täyttävän vaatimukset. Varmennusta varten diplomityön käytännönosuutena kehitetään varmennussovellus, joka suorittaa varmennuksen tietokannassa olevista arvoista.

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Neuropeptides affect the activity of the myriad of neuronal circuits in the brain. They are under tight spatial and chemical control and the dynamics of their release and catabolism directly modify neuronal network activity. Understanding neuropeptide functioning requires approaches to determine their chemical and spatial heterogeneity within neural tissue, but most imaging techniques do not provide the complete information desired. To provide chemical information, most imaging techniques used to study the nervous system require preselection and labeling of the peptides of interest; however, mass spectrometry imaging (MSI) detects analytes across a broad mass range without the need to target a specific analyte. When used with matrix-assisted laser desorption/ionization (MALDI), MSI detects analytes in the mass range of neuropeptides. MALDI MSI simultaneously provides spatial and chemical information resulting in images that plot the spatial distributions of neuropeptides over the surface of a thin slice of neural tissue. Here a variety of approaches for neuropeptide characterization are developed. Specifically, several computational approaches are combined with MALDI MSI to create improved approaches that provide spatial distributions and neuropeptide characterizations. After successfully validating these MALDI MSI protocols, the methods are applied to characterize both known and unidentified neuropeptides from neural tissues. The methods are further adapted from tissue analysis to be able to perform tandem MS (MS/MS) imaging on neuronal cultures to enable the study of network formation. In addition, MALDI MSI has been carried out over the timecourse of nervous system regeneration in planarian flatworms resulting in the discovery of two novel neuropeptides that may be involved in planarian regeneration. In addition, several bioinformatic tools are developed to predict final neuropeptide structures and associated masses that can be compared to experimental MSI data in order to make assignments of neuropeptide identities. The integration of computational approaches into the experimental design of MALDI MSI has allowed improved instrument automation and enhanced data acquisition and analysis. These tools also make the methods versatile and adaptable to new sample types.

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Orthopaedic infections can be polymicrobial existing as a microbiome. Infections often incorporate staphylococcal species, including Staphylococcus aureus. Such infections can lead to life threatening illness and implant failure. Furthermore, biofilm formation on the implant surface can occur, increasing pathogenicity, exacerbating antibiotic resistance and altering antimicrobial mechanism of action. Bacteria change dramatically during the transition to a biofilm growth state: phenotypically; transcriptionally; and metabolically, highlighting the need for research into molecular mechanisms involved in biofilm formation. Metabolomics can provide a tool to analyse metabolic changes which are directly related to the expressed phenotype. Here, we aimed to provide greater understanding of orthopaedic infection caused by S. aureus and biofilm formation on the implant surface. Through metagenome analysis by employing: implant material extraction; DNA extraction; microbial enrichment; and whole genome sequencing, we present a microbiome study of the infected prosthesis to resolve the causative species of orthopaedic hip infection. Results highlight the presence of S. aureus as a primary cause of orthopaedic infection along with Enterococcus faecium and the presence of secondary pathogen Clostridium difficile. Although results were hindered by the presence of host contaminating DNA even after microbial enrichment, conclusions could be made over the potential increased pathogenicity caused by the presence of a secondary pathogen and highlight method and sample preparation considerations when undertaking such a study. Following this finding, studies were focused on an orthopaedic clinical isolate of S. aureus and a metabolome extraction method for staphylococcal biofilms was developed using cell lysis through bead beating and solvent metabolome extraction. The method was found to be reproducible when coupled with liquid chromatography-mass spectrometry (LC-MS) and bioinformatics, allowing for the detection of significant changes in metabolism between planktonic and biofilm cultures to be identified and drug mechanism of actions (MOA) to be studied. Metabolomics results highlight significant changes in a number of metabolic pathways including arginine biosynthesis and purine metabolism between the two cell populations, evidence of S. aureus responding to their changing environment, including oxygen availability and a decrease in pH. Focused investigations on purine metabolism looking for biofilm modulation effects were carried out. Modulation of the S. aureus biofilm phenotype was observed through the addition of exogenous metabolites. Inosine increased biofilm biomass while formycin B, an inosine analogue, showed a dispersal effect and a potential synergistic effect in biofilm dispersal when coupled with gentamycin. Changes in metabolism between planktonic cells and biofilms highlight the requirement for antimicrobial testing to be carried out against planktonic cells and biofilms. Untargeted metabolomics was used to study the MOA of triclosan in S. aureus. The triclosan target and MOA in bacteria has already been characterised, however, questions remain over its effects in bacteria. Although the use of triclosan has come under increasing speculation, its full effects are still largely unknown. Results show that triclosan can induce a cascade of detrimental events in the cell metabolism including significant changes in amino acid metabolism, affecting planktonic cells and biofilms. Results and conclusions provide greater understanding of orthopaedic infections and specifically focus on the S. aureus biofilm, confirming S. aureus as a primary cause of orthopaedic infection and using metabolomic analysis to look at the changing state of metabolism between the different growth states. Metabolomics is a valuable tool for biofilm and drug MOA studies, helping understand orthopaedic infection and implant failure, providing crucial insight into the biochemistry of bacteria for the potential for inferences to be gained, such as the MOA of antimicrobials and the identification of novel metabolic drug targets.

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Due to the growth of design size and complexity, design verification is an important aspect of the Logic Circuit development process. The purpose of verification is to validate that the design meets the system requirements and specification. This is done by either functional or formal verification. The most popular approach to functional verification is the use of simulation based techniques. Using models to replicate the behaviour of an actual system is called simulation. In this thesis, a software/data structure architecture without explicit locks is proposed to accelerate logic gate circuit simulation. We call thus system ZSIM. The ZSIM software architecture simulator targets low cost SIMD multi-core machines. Its performance is evaluated on the Intel Xeon Phi and 2 other machines (Intel Xeon and AMD Opteron). The aim of these experiments is to: • Verify that the data structure used allows SIMD acceleration, particularly on machines with gather instructions ( section 5.3.1). • Verify that, on sufficiently large circuits, substantial gains could be made from multicore parallelism ( section 5.3.2 ). • Show that a simulator using this approach out-performs an existing commercial simulator on a standard workstation ( section 5.3.3 ). • Show that the performance on a cheap Xeon Phi card is competitive with results reported elsewhere on much more expensive super-computers ( section 5.3.5 ). To evaluate the ZSIM, two types of test circuits were used: 1. Circuits from the IWLS benchmark suit [1] which allow direct comparison with other published studies of parallel simulators.2. Circuits generated by a parametrised circuit synthesizer. The synthesizer used an algorithm that has been shown to generate circuits that are statistically representative of real logic circuits. The synthesizer allowed testing of a range of very large circuits, larger than the ones for which it was possible to obtain open source files. The experimental results show that with SIMD acceleration and multicore, ZSIM gained a peak parallelisation factor of 300 on Intel Xeon Phi and 11 on Intel Xeon. With only SIMD enabled, ZSIM achieved a maximum parallelistion gain of 10 on Intel Xeon Phi and 4 on Intel Xeon. Furthermore, it was shown that this software architecture simulator running on a SIMD machine is much faster than, and can handle much bigger circuits than a widely used commercial simulator (Xilinx) running on a workstation. The performance achieved by ZSIM was also compared with similar pre-existing work on logic simulation targeting GPUs and supercomputers. It was shown that ZSIM simulator running on a Xeon Phi machine gives comparable simulation performance to the IBM Blue Gene supercomputer at very much lower cost. The experimental results have shown that the Xeon Phi is competitive with simulation on GPUs and allows the handling of much larger circuits than have been reported for GPU simulation. When targeting Xeon Phi architecture, the automatic cache management of the Xeon Phi, handles and manages the on-chip local store without any explicit mention of the local store being made in the architecture of the simulator itself. However, targeting GPUs, explicit cache management in program increases the complexity of the software architecture. Furthermore, one of the strongest points of the ZSIM simulator is its portability. Note that the same code was tested on both AMD and Xeon Phi machines. The same architecture that efficiently performs on Xeon Phi, was ported into a 64 core NUMA AMD Opteron. To conclude, the two main achievements are restated as following: The primary achievement of this work was proving that the ZSIM architecture was faster than previously published logic simulators on low cost platforms. The secondary achievement was the development of a synthetic testing suite that went beyond the scale range that was previously publicly available, based on prior work that showed the synthesis technique is valid.

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We present the first case of gastro-intestinal perforation caused by a mint twig decorating a cocktail drink. A 76-year-old man was enjoying his Mojito cocktail on a cruise ship near Mexico when he accidently swallowed a mint twig, resulting in ileum perforation. This led to a cascade of events, eventually resulting in life-threatening multi-organ failure. Given this rare but potentially severe complication and the increasing popularity of decorated drinks, a less ‘fancy’ presentation for cocktails and similar drinks may be warranted.

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A ocratoxina A (OTA), micotoxina encontrada em diferentes níveis e em diversas matrizes, apresenta efeitos carcinogênicos, nefrotóxicos e teratogênicos. O desenvolvimento de métodos capazes de diminuir esta contaminação a níveis permitidos pela legislação é incentivado e os processos biológicos utilizados envolvem o uso de enzimas e/ou microrganismos para degradação da OTA e são preferenciais pela especificidade, bem como pelas condições brandas para a detoxificação. O objetivo do trabalho foi estudar a ação de carboxipeptidase A nos níveis e na toxicidade de OTA, visando aplicar a técnica para detoxificar farinhas de trigo. Primeiramente foi estimado o risco de exposição à ocratoxina A pelo consumo de farinhas de trigo. Para isso foram estabelecidas condições de determinação de OTA em farinhas de trigo, empregando técnicas de estatística multivariada para definir os principais interferentes na extração de OTA pelo método de QuEChERS e detecção em CLAE-FL. O método validado permitiu a avaliação da ocorrência natural em 20 amostras de farinha de trigo, estando estas contaminadas na faixa de 0,22 a 0,85 µg.kg-1 , apresentando um valor de ingestão diária de 0,08 ngOTA.dia-1 .kgmassacorpórea -1 e uma disponibilidade de 94,4%. Em seguida foi realizada a padronização da extração de carboxipeptidase A em biomassa de Rhizopus oryzae que consistiu em agitação ultrassônica durante 30 minutos numa potencia fixa de 150 W e 40 kHz e a triagem de agentes biológicos para degradação de OTA. Para o estudo da degradação in vitro de OTA, método de extração e detecção de OTA e OTα em CLAEFL foi validado e o processo de degradação foi realizado com Rhizopus oryzae e Trichoderma reesei, obtendo-se uma redução máxima de 63,5% e 57,7%, respectivamente. A degradação apresentou uma correlação alta (R>0,9) e significativa (p<0,05) com a produção de Otα, indicando que ocorreu a produção de enzimas capazes de hidrolisar a micotoxina, por exemplo, a carboxipeptidase A. O estudo da toxicidade de OTA e seu metabólito OTα foi realizado em neutrófilos humanos, onde foi observado a ausência de efeito tóxico de OTα. Também foi determinado o mecanismo de toxicidade de OTA pelo aumento de Ca2+ intracelular pela liberação a partir das reservas internas. Esta liberação, subsequentemente, provoca uma cascata de eventos, nomeadamente: a produção de espécies reativas, depleção de ATP, perda de ΔΨm, levando à morte por necrose. Para reduzir o risco de exposição à micotoxina pela ingestão de matéria prima contaminada, carboxipeptidase A extraída de diferentes fontes foi aplicada na hidrólise de OTA em farinha de trigo para posterior determinação do conteúdo residual de OTA e OTα, empregando método validado. O estudo mostrou uma redução de OTA entre 16,8 e 78,5% e produção de OTα entre 2 a 8,2 ng.g-1 . As carboxipeptidases mais promissoras para degradação foram as provenientes de Rhizopus e Trichoderma e a carboxipeptidase comercial. Ficou demonstrado que se pode recomendar a aplicação de enzimas proteolíticas, tipo carboxipeptidase, para reduzir o risco de exposição à micotoxina quando utilizada matéria prima contaminada, por exemplo, farinha de trigo para diferentes processos. A transformação de OTA para OTα e seus efeitos na redução da toxicidade da micotoxina corroboram com esta afirmação.

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10 p.

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ABSTRACT The Non-invasive Ventilation represents an alternative from ventilatory support, being frequently used in the treatment of respiratory failure. There are many complications associated with this technique, related to the pressure / air flow and the application of interfaces, being this one the focus of the article. The most appropriate interface selection allows a successful technique; the interface must be based on anatomical characteristics of the patient, cutaneous integrity and ventilation requirements. The Nurse plays a key role selecting the appropriate interface; technical monitoring and prevention of complications. The objective of the study is identify sensitive results to nursing care in the prevention of pressure ulcers (PPU) of the face, in adult and elderly submitted to NIV. This research was through EBSCO (CINAHL (Plus with Full Text) and MEDLINE (Plus with Full Text), with selection of full text articles between 2003-01-01 and 31.12.2013. We used the method of PI[C]O and was selected 13 articles from a total of 353. It was identified a set of specific interventions that prevent the appearing of pressure ulcer (PU), and according to Doran (2011), promotes sensitivity to nursing care results. The nursing interventions in adults with NIV have a direct impact on health outcomes, with preventing and resolving complications, with contribution in terms of effective disease control, adherence to the treatment regimen and consequent increase in life quality.

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Among the psychiatric diseases, bipolar disorder (BD) is the sixth leading cause of disability with a prevalence up to 4 % worldwide. BD is a complex neuropsychiatric condition which alternates episodes of mania with symptoms of depression. Although the neurobiological pathways are not completely clarified, the dopamine (DA) hypothesis, recognized as the leading theory explaining the pathophysiology of the malady, states that the dramatically compromised homeostatic regulation of dopaminergic circuits leads to alternated changes in DA neurotransmission. Modulation of D2 and D3 receptors (D2/3R) through partial agonists represents the first-line therapeutic strategy for psychiatric diseases. Moreover, a deregulation of the enzyme glycogen synthase kinase-3β (GSK-3β) has been reported as peculiar feature of BD. In this scenario, the concomitant modulation of D3R and GSK-3β, by employing multitarget compounds, could offer promises to achieve an effective cure of this illness. In the light of these findings, we rationally envisaged the pharmacophoric model at the basis of the design of several D3R partial agonists, suitable to be exploited for the dual D3R/GSK-3β ligand design. Thus, synthetic efforts were addressed to develop a first set of hybrid molecules able to concurrently modulate the selected targets. For a chemical structure point of view, we employed different spacers to combine a substituted aryl-piperazine moiety, reported in previously discovered D3R modulators, with a pyrazole-based fragment, already identified in GSK-3β inhibitors. A fluorescent and a cellular functional assays were carried out to assess the activity of all synthetized compounds against GSK-3β and on D3R, respectively. Most of the derivatives proved to effectively modulate both GSK-3β and D3R with potencies in the low-µM and low-nM range, respectively. The consistent biological data allowed us to identify some lead candidates worth to be further modified with the aim to optimize their biological profile and to perform a structure-activity relationship (SAR) study.

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Previous studies have shown that zinc deficiency leads to apoptosis of neuronal precursor cells in vivo and in vitro. In addition to the role of p53 as a nuclear transcription factor in zinc deficient cultured human neuronal precursors (NT-2), we have now identified the translocation of phosphorylated p53 to the mitochondria and p53-dependent increases in the pro-apoptotic mitochondrial protein BAX leading to a loss of mitochondrial membrane potential as demonstrated by a 25% decrease in JC-1 red:green fluorescence ratio. Disruption of mitochondrial membrane integrity was accompanied by efflux of the apoptosis inducing factor (AIF) from the mitochondria and translocation to the nucleus with a significant increase in reactive oxygen species (ROS) after 24 h of zinc deficiency. Measurement of caspase cleavage, mRNA, and treatment with caspase inhibitors revealed the involvement of caspases 2, 3, 6, and 7 in zinc deficiency-mediated apoptosis. Down-stream targets of caspase activation, including the nuclear structure protein lamin and polyADP ribose polymerase (PARP), which participates in DNA repair, were also cleaved. Transfection with a dominant-negative p53 construct and use of the p53 inhibitor, pifithrin- ␮, established that these alterations were largely dependent on p53. Together these data identify a cascade of events involving mitochondrial p53 as well as p53-dependent caspase-mediated mechanisms leading to apoptosis during zinc deficiency.