996 resultados para Luminescence mechanisms


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Electrochemical investigations were conducted of the effect of potential on the luminescence of porous silico (PS). The use of liquid contacts allows the potential to be controlled during studies of the photoluminescence (PL) and electroluminescence (EI). The PL and EL of PS samples prepared from n-type substrates is considered. To obtain luminescence from such PS it is necessary to generate holes in the valence band. This is achieved by either photoexcitation or an electrochemical process involving the reduction of persulfate. This paper describes the investigations of the effect of potential on the PL and EL of PS. A mechanism of 'potential tuning' based on electron occupancy and Auger quenching is then proposed.

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In this paper, the static and dynamic performance of multi quantum-well (MQW) 1.3 μm InGaAsP Fabry Perot lasers is assessed experimentally and theoretically to identify the mechanisms responsible for impaired high speed performance at elevated temperature. Initially, threshold currents and spontaneous emission spectra are characterized for a range of temperatures from room temperature to 85 °C to indicate a significant increase in non-radiative current contributions. Preliminary estimates are made for the contributions of leakage and Auger recombination rates, found from the dependence of integrated spontaneous emission with carrier density. Drift-diffusion modelling is found to accurately predict the trend of threshold currents over temperature. Using gain modelling good agreement is found between the measured and predicted integrated spontaneous emission intensity. Gain measurements at 85 °C indicate a reduction in RIN frequency to 63% of the 25 °C value which matches well with experimental small signal performance.

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In the field of flat panel displays, the current leading technology is the Active Matrix liquid Crystal Display; this uses a-Si:H based thin film transistors (TFTs) as the switching element in each pixel. However, under gate bias a-Si:H TFTs suffer from instability, as is evidenced by a shift in the gate threshold voltage. The shift in the gate threshold voltage is generally measured from the gate transfer characteristics, after subjecting the TFT to prolonged gate bias. However, a major drawback of this measurement method is that it cannot distinguish whether the shift is caused by the change in the midgap states in the a-Si:H channel or by charge trapping in the gate insulator. In view of this, we have developed a capacitance-voltage (C-V) method to measure the shift in threshold voltage. We employ Metal-Insulator-Semiconductor (MIS) structures to investigate the threshold voltage shift as they are simpler to fabricate than TFTs. We have investigated a large of number Metal/a-Si:H/Si3N4/Si+n structures using our C-V technique. From, the C-V data for the MIS structures, we have found that the relationship between the thermal energy and threshold voltage shift is similar to that reported by Wehrspohn et. al in a-Si:H TFTs (J Appl. Phys, 144, 87, 2000). The a-Si:H and Si3N4 layers were grown using the radio-frequency plasma-enhanced chemical vapour deposition technique.

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We have investigated the karyotype relationships of two oriental voles, i.e. the Yulong vole (Eothenomys proditor, 2n = 32) and the large oriental vole (Eothenomys miletus, 2n = 56) as well as the Clarke's vole (Microtus clarkei, 2n = 52), by a combined a

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In reciprocal mutualism systems, the exploitation events by exploiters might disrupt the reciprocal mutualism, wherein one exploiter species might even exclude other coexisting exploiter species over an evolutionary time frame. What remains unclear is how such a community is maintained. Niche partitioning, or spatial heterogeneity among the mutualists and exploiters, is generally believed to enable stability within a mutualistic system. However, our examination of a reciprocal mutualism between a fig species (Ficus racemosa) and its pollinator wasp (Ceratosolen fusciceps) shows that spatial niche partitioning does not sufficiently prevent exploiters from overexploiting the common resource (i.e., the female flowers), because of the considerable niche overlap between the mutualists and exploiters. In response to an exploiter, our experiment shows that the fig can (1) abort syconia-containing flowers that have been galled by the exploiter, Apocryptophagus testacea, which oviposits before the pollinators do; and (2) retain syconia-containing flowers galled by Apocryptophagus mayri, which oviposit later than pollinators. However, as a result of (2), there is decreased development of adult non-pollinators or pollinator species in syconia that have not been sufficiently pollinated, but not aborted. Such discriminative abortion of figs or reduction in offspring development of exploiters while rewarding cooperative individuals with higher offspring development by the fig will increase the fitness of cooperative pollinating wasps, but decrease the fitness of exploiters. The fig fig wasp interactions are diffusively coevolved, a case in which fig wasps diversify their genotype, phenotype, or behavior as a result of competition between wasps, while figs diverge their strategies to facilitate the evolution of cooperative fig waps or lessen the detrimental behavior by associated fig wasps. In habitats or syconia that suffer overexploitation, discriminative abortion of figs or reduction in the offspring development of exploiters in syconia that are not or not sufficiently pollinated will decrease exploiter fitness and perhaps even drive the population of exploiters to local extinction, enabling the evolution and maintenance of cooperative pollinators through the movement between habitats or syconia (i.e., the metapopulations).

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Bone marrow-derived mesenchymal stem cells (MSCs) hold great promise for treating immune disorders because of their immunoregulatory capacity, but the mechanism remains controversial. As we show here, the mechanism of MSC-mediated immunosuppression varies

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Recently, we demonstrated that humans can learn to make accurate movements in an unstable environment by controlling magnitude, shape, and orientation of the endpoint impedance. Although previous studies of human motor learning suggest that the brain acquires an inverse dynamics model of the novel environment, it is not known whether this control mechanism is operative in unstable environments. We compared learning of multijoint arm movements in a "velocity-dependent force field" (VF), which interacted with the arm in a stable manner, and learning in a "divergent force field" (DF), where the interaction was unstable. The characteristics of error evolution were markedly different in the 2 fields. The direction of trajectory error in the DF alternated to the left and right during the early stage of learning; that is, signed error was inconsistent from movement to movement and could not have guided learning of an inverse dynamics model. This contrasted sharply with trajectory error in the VF, which was initially biased and decayed in a manner that was consistent with rapid feedback error learning. EMG recorded before and after learning in the DF and VF are also consistent with different learning and control mechanisms for adapting to stable and unstable dynamics, that is, inverse dynamics model formation and impedance control. We also investigated adaptation to a rotated DF to examine the interplay between inverse dynamics model formation and impedance control. Our results suggest that an inverse dynamics model can function in parallel with an impedance controller to compensate for consistent perturbing force in unstable environments.

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Humans have exceptional abilities to learn new skills, manipulate tools and objects, and interact with our environment. In order to be successful at these tasks, our brain has developed learning mechanisms to deal with and compensate for the constantly changing dynamics of the world. If this mechanism or mechanisms can be understood from a computational point of view, then they can also be used to drive the adaptability and learning of robots. In this paper, we will present a new technique for examining changes in the feedforward motor command due to adaptation. This technique can then be utilized for examining motor adaptation in humans and determining a computational algorithm which explains motor learning. © 2007.

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The Internet of Things (IOT) concept and enabling technologies such as RFID offer the prospect of linking the real world of physical objects with the virtual world of information technology to improve visibility and traceability information within supply chains and across the entire lifecycles of products, as well as enabling more intuitive interactions and greater automation possibilities. There is a huge potential for savings through process optimization and profit generation within the IOT, but the sharing of financial benefits across companies remains an unsolved issue. Existing approaches towards sharing of costs and benefits have failed to scale so far. The integration of payment solutions into the IOT architecture could solve this problem. We have reviewed different possible levels of integration. Multiple payment solutions have been researched. Finally we have developed a model that meets the requirements of the IOT in relation to openness and scalability. It supports both hardware-centric and software-centric approaches to integration of payment solutions with the IOT. Different requirements concerning payment solutions within the IOT have been defined and considered in the proposed model. Possible solution providers include telcos, e-payment service providers and new players such as banks and standardization bodies. The proposed model of integrating the Internet of Things with payment solutions will lower the barrier to invoicing for the more granular visibility information generated using the IOT. Thus, it has the potential to enable recovery of the necessary investments in IOT infrastructure and accelerate adoption of the IOT, especially for projects that are only viable when multiple benefits throughout the supply chain need to be accumulated in order to achieve a Return on Investment (ROI). In a long-term perspective, it may enable IT-departments to become profit centres instead of cost centres. © 2010 - IOS Press and the authors. All rights reserved.

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Learning and memory are exquisitely sensitive to behavioral stress, but the underlying mechanisms are still poorly understood. Because activity-dependent persistent changes in synaptic strength are believed to mediate memory processes in brain areas such as the hippocampus we have examined the means by which stress affects synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats, Inescapable behavioral stress (placement on an elevated platform for 30 min) switched the direction of plasticity, favoring low frequency stimulation-induced decreases in synaptic transmission (long-term depression, LTD), and opposing the induction of long-term potentiation by high frequency stimulation, We have discovered that glucocorticoid receptor activation mediates these effects of stress on LTD and longterm potentiation in a protein synthesis-dependent manner because they were prevented by the glucocorticoid receptor antagonist RU 38486 and the protein synthesis inhibitor emetine. Consistent with this, the ability of exogenously applied corticosterone in non-stressed rats to mimic the effects of stress on synaptic plasticity was also blocked by these agents, The enablement of low frequency stimulation-induced LTD by both stress and exogenous corticosterone was also blocked by the transcription inhibitor actinomycin D, Thus, naturally occurring synaptic plasticity is liable to be reversed in stressful situations via glucocorticoid receptor activation and mechanisms dependent on the synthesis of new protein and RNA, This indicates that the modulation of hippocampus-mediated learning by acute inescapable stress requires glucocorticoid receptor-dependent initiation of transcription and translation.

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Many ionotropic receptors are modulated by extracellular H+. So far, few studies have directly addressed the role of such modulation at synapses. In the present study, we investigated the effects of changes in extracellular pH on glycinergic miniature inhibitory postsynaptic currents (mIPSCs) as well as glycine-evoked currents (I-Gly) in mechanically dissociated spinal neurons with native synaptic boutons preserved. H+ modulated both the mIPSCs and I-Gly, biphasically, although it activated an amiloride-sensitive inward current by itself. Decreasing extracellular pH reversibly inhibited the amplitude of the mIPSCs and I-Gly, while increasing external pH reversibly potentiated these parameters. Blockade of acid-sensing ion channels (ASICs) with amiloride, the selective antagonist of ASICs, or decreasing intracellular pH did not alter the modulatory effect of H+ on either mIPSCs or I-Gly, H+ shifted the EC50 of the glycine concentration-response curve from 49.3 +/- 5.7 muM at external pH 7.4 to 131.5 +/- 8.1 muM at pH 5.5, without altering the Cl- selectivity of the glycine receptor (GlyR), the Hill coefficient and the maximal I-Gly, suggesting a competitive inhibition of I-Gly by H+. Both Zn2+ and H+ inhibited I-Gly. However, H+ induced no further inhibition of I-Gly in the presence of a saturating concentration of Zn2+. In addition, H+ significantly affected the kinetics of glycinergic mIPSCs and I-Gly. It is proposed that H+ and/or Zn2+ compete with glycine binding and inhibit the amplitude of glycinergic mIPSCs and I-Gly. Moreover, binding of H+ induces a global conformational change in GlyR, which closes the GlyR Cl- channel and results in the acceleration of the seeming desensitization of IGly as well as speeding up the decay time constant of glycinergic mIPSCs. However, the deprotonation rate is faster than the unbinding rate of glycine from the GlyR, leading to reactivation of the undesensitized GlyR after washout of agonist and the appearance of a rebound I-Gly. H+ also modulated the glycine cotransmitter, GABA-activated current (I-GABA). Taken together, the results support a 'conformational coupling' model for H+ modulation of the GlyR and suggest that W may act as a novel modulator for inhibitory neurotransmission in the mammalian spinal cord.

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The hippocampus, being sensitive to stress and glucocorticoids, plays significant roles in certain types of learning and memory. Therefore, the hippocampus is probably involved in the increasing drug use, drug seeking, and relapse caused by stress. We have studied the effect of stress with morphine on synaptic plasticity in the CA1 region of the hippocampus in vivo and on a delayed-escape paradigm of the Morris water maze. Our results reveal that acute stress enables long-term depression (LTD) induction by low-frequency stimulation (LFS) but acute morphine causes synaptic potentiation. Remarkably, exposure to an acute stressor reverses the effect of morphine from synaptic potentiation ( similar to 20%) to synaptic depression ( similar to 40%), precluding further LTD induction by LFS. The synaptic depression caused by stress with morphine is blocked either by the glucocorticoid receptor antagonist RU38486 or by the NMDA-receptor antagonist D-APV. Chronic morphine attenuates the ability of acute morphine to cause synaptic potentiation, and stress to enable LTD induction, but not the ability of stress in tandem with morphine to cause synaptic depression. Furthermore, corticosterone with morphine during the initial phase of drug use promotes later delayed-escape behavior, as indicated by the morphine-reinforced longer latencies to escape, leading to persistent morphine-seeking after withdrawal. These results suggest that hippocampal synaptic plasticity may play a significant role in the effects of stress or glucocorticoids on opiate addiction.