974 resultados para heterodyne interference


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The plane wave electromagnetic interference (EMI) shielding properties of DC sputtered Ni79Fe16Mo5 and copper layers were studied according to ASTM D 4935-89 on frequency range of 50 MHz – 2.5 GHz and RF magnetic shielding effectiveness by shielded magnetic loop probes. Results show that Ni79Fe16Mo5 provides better RF magnetic shielding above the layer thickness of approximately 120 nm. Copper provides better plane wave shielding effectiveness. The effect of shield internal interfaces was studied by depositing thin multilayer structures with and without a dielectric spacer layer.

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Les syndromes de déficiences cérébrales en créatine (CCDS) sont dus à des mutations dans les gènes GATM et G AMT (codant pour les enzymes AGAT et G AMT de la voie de synthèse de créatine) ainsi que SLC6A8 (transporteur de créatine), et génèrent une absence ou une très forte baisse de créatine (Cr) dans le cerveau, mesurée par spectroscopic de résonance magnétique. Les patients CCDS développent des handicaps neurologiques sévères. Les patients AGAT et GAMT peuvent être traités avec des doses importantes de Cr, mais gardent dans la plupart des cas des séquelles neurologiques irréversibles. Aucun traitement efficace n'existe à ce jour pour la déficience en SLC6A8. Bien que de nombreux modèles aient été développés pour comprendre la Cr cérébrale en conditions physiologiques, les pathomécanismes des CCDS ne sont pas encore compris. Des souris transgéniques pour les gènes Gatm, Gamt et Slc6a8 ont été générées, mais elles ne miment que partiellement la pathologie humaine. Parmi les CCDS, la déficience en GAMT est la plus sévère, en raison de l'accumulation cérébrale de l'intermédiaire guanidinoacétate (GAA). Alors que la toxicité cérébrale du GAA a été étudiée par exposition directe au GAA d'animaux adultes sains, les mécanismes de la toxicité du GAA en condition de déficience en GAMT dans le cerveau en développement sont encore inconnus. Le but de ce projet était donc de développer un modèle de déficience en GAMT dans des cultures 3D primaires de cellules nerveuses de rat en agrégats par knock-down du gène GAMT, en utilisant un virus adéno-associé (AAV) induisant le mécanisme d'interférence à l'ARN (RNAi). Le virus scAAV2, à la multiplicité d'infection de 1000, s'est révélé le plus efficace pour transduire tous les types de cellules nerveuses des cultures (neurones, astrocytes, oligodendrocytes), et générer un knock-down maximal de la protéine GAMT de 85% (jour in vitro 18). Cette déficience partielle en GAMT s'est révélée insuffisante pour générer une déficience en Cr, mais a causé l'accumulation attendue de GAA, à des doses comparables aux niveaux observés dans le LCR des patients GAMT. Le GAA a induit une croissance axonale anarchique accompagnée d'une baisse de l'apoptose naturelle, suivis par une induction tardive de mort cellulaire non-apoptotique. Le co-traitement par la Cr a prévenu tous les effets toxiques du GAA. Ce travail montre que l'accumulation de GAA en absence de déficience en Cr est suffisante pour affecter le développement du tissu nerveux, et suggère que des formes de déficiences en GAMT supplémentaires, ne présentant pas de déficiences en Cr, pourraient être découvertes par mesure du GAA, en particulier à travers les programmes récemment proposés de dépistage néonatal de la déficience en GAMT. -- Cerebral creatine deficiency syndromes (CCDS) are caused by mutations in the genes GATM and GAMT (respectively coding for the two enzymes of the creatine synthetic pathway, AGAT and GAMT) as well as SLC6A8 (creatine transporter), and lead to the absence or very strong decrease of creatine (Cr) in the brain when measured by magnetic resonance spectroscopy. Affected patients show severe neurological impairments. While AGAT and GAMT deficient patients can be treated with high dosages of Cr, most remain with irreversible brain sequelae. No treatment has been successful so far for SLC6A8 deficiency. While many models have helped understanding the cerebral Cr pathways in physiological conditions, the pathomechanisms underlying CCDS are yet to be elucidated. Transgenic mice carrying mutations in the Gatm, Gamt and Slc6a8 genes have been developed, but only partially mimic the human pathology. Among CCDS, GAMT deficiency is the most severe, due to the CNS accumulation of the guanidinoacetate (GAA) intermediate. While brain toxicity of GAA has been explored through direct GAA exposure of adult healthy animals, the mechanisms underlying GAA toxicity in GAMT deficiency conditions on the developing CNS are yet unknown. The aim of this project was thus to develop and characterize a GAMT deficiency model in developing brain cells by gene knockdown, by adeno-associated virus (AAV)-driven RNA interference (RNAi) in rat 3D organotypic primary brain cell cultures in aggregates. scAAV2 with a multiplicity of infection of 1000 was shown as the most efficient serotype, was able to transduce all brain cell types (neurons, astrocytes, oligodendrocytes) and to induce a maximal GAMT protein knockdown of 85% (day in vitro 18). Metabolite analysis showed that partial GAMT knockdown was insufficient to induce Cr deficiency but generated the awaited GAA accumulation at concentrations comparable to the levels observed in cerebrospinal fluid of GAMT-deficient patients. Accumulated GAA induced axonal hypersprouting paralleled with inhibition of natural apoptosis, followed by a later induction in non-apoptotic cell death. Cr supplementation led to the prevention of all GAA-induced toxic effects. This work shows that GAA accumulation without Cr deficiency is sufficient to affect CNS development, and suggests that additional partial GAMT deficiencies, which may not show the classical brain Cr deficiency, may be discovered through GAA measurement including by recently proposed neonatal screening programs for GAMT deficiency.

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This study uses event-related brain potentials (ERPs) to investigate the electrophysiological correlates of numeric conflict monitoring in math-anxious individuals, by analyzing whether math anxiety is related to abnormal processing in early conflict detection (as shown by the N450 component) and/or in a later, response-related stage of processing (as shown by the conflict sustained potential; Conflict-SP). Conflict adaptation effects were also studied by analyzing the effect of the previous trial"s congruence in current interference. To this end, 17 low math-anxious (LMA)and 17 high math-anxious (HMA) individuals were presented with a numerical Stroop task. Groups were extreme in math anxiety but did not differ in trait or state anxiety or in simple math ability. The interference effect of the current trial (incongruent-congruent) and the interference effect preceded by congruence and by incongruity were analyzed both for behavioral measures and for ERPs. A greater interference effect was found for response times in the HMA group than in the LMA one. Regarding ERPs, the LMA group showed a greater N450 component for the interference effect preceded by congruence than when preceded by incongruity, while the HMA group showed greater Conflict-SP amplitude for the interference effect preceded by congruence than when preceded by incongruity. Our study showed that the electrophysiological correlates of numeric interference in HMA individuals comprise the absence of a conflict adaptation effect in the first stage of conflict processing (N450) and an abnormal subsequent up-regulation of cognitive control in order to overcome the conflict (Conflict-SP). More concretely, our study shows that math anxiety is related to a reactive and compensatory recruitment of control resources that is implemented only when previously exposed to a stimuli presenting conflicting information

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We had described that epidermal growth factor (EGF) interfered with the lipolytic effect of catecholamines in isolated adipocytes. Since catecholamines stimulate the release of EGF from submandibular salivary glands to blood plasma in male mice, we studied whether EGF affected also the lipolytic response to adrenaline in whole animals. We studied the effect of adrenaline in sialoadenectomized and sham-operated mice receiving or not a high dose of EGF following adrenaline injection. There was no difference in plasma EGF concentration between sham-operated and sialoadenectomized animals receiving saline. After adrenaline administration plasma EGF increased by 20-fold in sham-operated but did not increase in sialoadenectomized mice. Indeed, the increase was much higher (more than 100-fold) in mice receiving exogenous EGF. The effect of adrenaline on plasma concentration of both glycerol and nonesterified fatty acids was higher as lower was plasma EGF concentration. Isolated adipocytes obtained from sham-operated or sialoadenectomized mice had identical lipolytic response to adrenaline. The lipolytic response of adipocytes to isoproterenol was decreased by addition of EGF. To study whether the interference with the in vivo lipolytic effect of adrenaline had further metabolic consequences, we measured plasma b-hydroxybutyrate concentration in plasma. There was no difference in the response to adrenaline between sham-operated and sialoadenectomized mice in spite of the difference in plasma nonsterified fatty acid concentration. Studies in isolated hepatocytes indicated that ketogenesis run at near maximal rate in this range of substrate concentration. These results suggest that EGF in the physiological range decreases the lipolytic effect of adrenaline but does not compromise further metabolic events like the enhancement of ketogenesis.

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Mitochondria has an essential role in myocardial tissue homeostasis; thus deterioration in mitochondrial function eventually leads to cardiomyocyte and endothelial cell death and consequent cardiovascular dysfunction. Several chemical compounds and drugs have been known to directly or indirectly modulate cardiac mitochondrial function, which can account both for the toxicological and pharmacological properties of these substances. In many cases, toxicity problems appear only in the presence of additional cardiovascular disease conditions or develop months/years following the exposure, making the diagnosis difficult. Cardiotoxic agents affecting mitochondria include several widely used anticancer drugs [anthracyclines (Doxorubicin/Adriamycin), cisplatin, trastuzumab (Herceptin), arsenic trioxide (Trisenox), mitoxantrone (Novantrone), imatinib (Gleevec), bevacizumab (Avastin), sunitinib (Sutent), and sorafenib (Nevaxar)], antiviral compound azidothymidine (AZT, Zidovudine) and several oral antidiabetics [e.g., rosiglitazone (Avandia)]. Illicit drugs such as alcohol, cocaine, methamphetamine, ecstasy, and synthetic cannabinoids (spice, K2) may also induce mitochondria-related cardiotoxicity. Mitochondrial toxicity develops due to various mechanisms involving interference with the mitochondrial respiratory chain (e.g., uncoupling) or inhibition of the important mitochondrial enzymes (oxidative phosphorylation, Szent-Györgyi-Krebs cycle, mitochondrial DNA replication, ADP/ATP translocator). The final phase of mitochondrial dysfunction induces loss of mitochondrial membrane potential and an increase in mitochondrial oxidative/nitrative stress, eventually culminating into cell death. This review aims to discuss the mechanisms of mitochondrion-mediated cardiotoxicity of commonly used drugs and some potential cardioprotective strategies to prevent these toxicities.

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In the peripheral sensory nervous system the neuronal expression of voltage-gated sodium channels (Navs) is very important for the transmission of nociceptive information since they give rise to the upstroke of the action potential (AP). Navs are composed of nine different isoforms with distinct biophysical properties. Studying the mutations associated with the increase or absence of pain sensitivity in humans, as well as other expression studies, have highlighted Nav1.7, Nav1.8, and Nav1.9 as being the most important contributors to the control of nociceptive neuronal electrogenesis. Modulating their expression and/or function can impact the shape of the AP and consequently modify nociceptive transmission, a process that is observed in persistent pain conditions. Post-translational modification (PTM) of Navs is a well-known process that modifies their expression and function. In chronic pain syndromes, the release of inflammatory molecules into the direct environment of dorsal root ganglia (DRG) sensory neurons leads to an abnormal activation of enzymes that induce Navs PTM. The addition of small molecules, i.e., peptides, phosphoryl groups, ubiquitin moieties and/or carbohydrates, can modify the function of Navs in two different ways: via direct physical interference with Nav gating, or via the control of Nav trafficking. Both mechanisms have a profound impact on neuronal excitability. In this review we will discuss the role of Protein Kinase A, B, and C, Mitogen Activated Protein Kinases and Ca++/Calmodulin-dependent Kinase II in peripheral chronic pain syndromes. We will also discuss more recent findings that the ubiquitination of Nav1.7 by Nedd4-2 and the effect of methylglyoxal on Nav1.8 are also implicated in the development of experimental neuropathic pain. We will address the potential roles of other PTMs in chronic pain and highlight the need for further investigation of PTMs of Navs in order to develop new pharmacological tools to alleviate pain.

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Concomitant aortic and mitral valve replacement or concomitant aortic valve replacement and mitral repair can be a challenge for the cardiac surgeon: in particular, because of their structure and design, two bioprosthetic heart valves or an aortic valve prosthesis and a rigid mitral ring can interfere at the level of the mitroaortic junction. Therefore, when a mitral bioprosthesis or a rigid mitral ring is already in place and a surgical aortic valve replacement becomes necessary, or when older high-risk patients require concomitant mitral and aortic procedures, the new 'fast-implantable' aortic valve system (Intuity valve, Edwards Lifesciences, Irvine, CA, USA) can represent a smart alternative to standard aortic bioprosthesis. Unfortunately, this is still controversial (risk of interference). However, transcatheter aortic valve replacements have been performed in patients with previously implanted mitral valves or mitral rings. Interestingly, we learned that there is no interference (or not significant interference) among the standard valve and the stent valve. Consequently, we can assume that a fast-implantable valve can also be safely placed next to a biological mitral valve or next to a rigid mitral ring without risks of distortion, malpositioning, high gradient or paravalvular leak. This paper describes two cases: a concomitant Intuity aortic valve and bioprosthetic mitral valve implantation and a concomitant Intuity aortic valve and mitral ring implantation.

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Durante toda la evolución de la tecnología, se han empleado aparatos interconexionados por cables. Los cables limitan la libertad de movimiento del usuario y pueden captar interferencias entre ellos si la red de cableado es elevada. Mientras avanzaba la tecnología inalámbrica, se ha ido adaptando al equipamiento electrónico a la vez que se iban haciendo cada vez más pequeños. Por esto, se impone la necesidad de utilizarlos como controles a distancia sin el empleo de cables debido a los inconvenientes que estos conllevan. El presente trabajo, pretende unificar tres tecnologías que pueden tener en el futuro una gran afinidad. · Dispositivos basados en el sistema Android. Desde sus inicios, han tenido una evolución meteórica. Se han ido haciendo cada vez más rápidos y mejores. · Sistemas inalámbricos. Los sistemas wifi o bluetooth, se han ido incorporando a nuestras vidas cada vez más y están prácticamente en cualquier aparato. · Robótica. Cualquier proceso de producción incorpora un robot. Son necesarios para hacer muchos trabajos que, aunque el hombre lo puede realizar, un robot reduce los tiempos y la peligrosidad de los procesos. Aunque las dos primeras tecnologías van unidas, ¿quién no tiene un teléfono con conexión wifi y bluetooth?, pocos diseños aúnan estos campos con la Robótica. El objetivo final de este trabajo es realizar una aplicación en Android para el control remoto de un robot, empleando el sistema de comunicación inalámbrico. La aplicación desarrollada, permite controlar el robot a conveniencia del usuario en un entorno táctil/teledirigido. Gracias a la utilización de simulador en ambos lenguajes (RAPID y Android), ha sido posible realizar la programación sin tener que estar presente ante el robot objeto de este trabajo. A través de su progreso, se ha ido evolucionando en la cantidad de datos enviados al robot y complejidad en su procesamiento, a la vez que se ha mejorado en la estética de la aplicación. Finalmente se usó la aplicación desarrollada con el robot, consiguiendo con éxito que realizara los movimientos que eran enviados con la tablet programada.

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The issue of how contractility and adhesion are related to cell shape and migration pattern remains largely unresolved. In this paper we report that Gleevec (Imatinib), an Abl family kinase inhibitor, produces a profound change in the shape and migration of rat bladder tumor cells (NBTII) plated on collagen-coated substrates. Cells treated with Gleevec adopt a highly spread D-shape and migrate more rapidly with greater persistence. Accompanying this more spread state is an increase in integrin-mediated adhesion coupled with increases in the size and number of discrete adhesions. In addition, both total internal reflection fluorescence microscopy (TIRFM) and interference reflection microscopy (IRM) revealed a band of small punctate adhesions with rapid turnover near the cell leading margin. These changes led to an increase in global cell-substrate adhesion strength, as assessed by laminar flow experiments. Gleevec-treated cells have greater RhoA activity which, via myosin activation, led to an increase in the magnitude of total traction force applied to the substrate. These chemical and physical alterations upon Gleevec treatment produce the dramatic change in morphology and migration that is observed.

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Expression of the SS18/SYT-SSX fusion protein is believed to underlie the pathogenesis of synovial sarcoma (SS). Recent evidence suggests that deregulation of the Wnt pathway may play an important role in SS but the mechanisms whereby SS18-SSX might affect Wnt signaling remain to be elucidated. Here, we show that SS18/SSX tightly regulates the elevated expression of the key Wnt target AXIN2 in primary SS. SS18-SSX is shown to interact with TCF/LEF, TLE and HDAC but not β-catenin in vivo and to induce Wnt target gene expression by forming a complex containing promoter-bound TCF/LEF and HDAC but lacking β-catenin. Our observations provide a tumor-specific mechanistic basis for Wnt target gene induction in SS that can occur in the absence of Wnt ligand stimulation.

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Among invasive species, ants are a particularly prominent group with enormous impacts on native biodiversity and ecosystem functioning. Globalization and on-going climate change are likely to increase the rate of ant invasions in the future, leading to simultaneous introductions of several highly invasive species within the same area, Here, we investigate pairwise interactions among four highly invasive species, Linepithema humile,Lashis neglectus, Pheidole megacephala and Wasmannia auropunctata, at the whole colony level, using a laboratory set-up. :Each colony consisted of 300 workers and one queen. The number of surviving workers in the competing colonies was recorded daily over 7 weeks. We modelled the survival of each colony during pairwise colony interactions, using a nonlinear model characterizing the survival dynamics of each colony individually. The least dominant species was P. megacephala, which always went extinct. Interactions among the three other species showed more complex dynamics, rendering the outcome of the interactions less predictable. Overall, W auropunctata and L neglectus were the most dominant species. This study shows the importance of scaling up to the colony level in order to gain realism in predicting the outcome of multiple invasions.

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The Potentiometric Stripping Analysis (PSA) is described with emphasis on ultramicroelectrode applications with a laboratory developed computer based instrumentation. The technique potentialities as compared with the voltammetric approach are pointed out based on the current literature. Some results of trace metals analysis including zinc, cadmium, lead and copper in vinegar and canned food samples are presented. The mainly advantage found in our laboratory was the technique capability to analyse natural samples with minimum matrix interference and the low level of noise found in our determinations.

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The determination of zirconium-hafnium mixtures is one of the most critical problem of the analytical chemistry, on account of the close similarity of their chemical properties. The spectrophotometric determination proposed by Yagodin et al. show not many practical applications due to the significant spectral interference on the 200-220 nm region. In this work we propound the use of a multivariate calibration method called partial least squares ( PLS ) for colorimetric determination of these mixtures. By using PLS and 16 calibration mixtures we obtained a model which permits determination of zirconium and hafnium with accuracy of about 1-2% and 10-20%, respectively. Using conventional univariate calibration the inaccuracy of the determination is about 10-25% for zirconium and above 57% for hafnium.

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The aim of this work is to study the electrochromism and the reaction kinetics of lithium electrointercalation in anodic niobium oxide films. The oxide grown in an acid environment by application of an alternating potential shows interference colour (iridescence) and when reduced in lithium perclorate/PC solution, the intercalation of Li+ ions and electrons causes a reversible colour change (electrochromism), characterized here by electrochemical and optical measurements. A model where the reaction kinetics is dominated by diffusion of ionic pairs (Li+, e-) in the oxide film permitted the reproduction of current and absorbance temporal dependence, confirming the relationship between the electrochromic and electrochemical reactions. From the results obtained, a relation was established where the colour change is associated to the reduction of Nb+5 to Nb+4 ions with simultaneous cations injection.

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X-This work shows an alternative method to copper determination by X-Ray Fluorescence (XRF). Since copper concentration in natural waters is not enough to reach XRF detection limit, a liquid-solid preconcentration procedure was proposed. Glycerin was used to complex the metal increasing its adsorption on activated charcoal. The solid phase was used to XRF determination. Several parameters were evaluated, such as, the complexation pH, the charcoal adsorption limit and the glycerin concentration. The interferences are lead and bismuth and the sensitivities decreased in the order Cu2+, Bi3+ and Pb2+. The advantages of the method are its simplicity, low cost and low spectral interference.