634 resultados para Epstein, AbrahamEpstein, AbrahamAbrahamEpstein


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Each stage in the life cycle of coal-extraction, transport, processing, and combustion-generates a waste stream and carries multiple hazards for health and the environment. These costs are external to the coal industry and are thus often considered "externalities." We estimate that the life cycle effects of coal and the waste stream generated are costing the U.S. public a third to over one-half of a trillion dollars annually. Many of these so-called externalities are, moreover, cumulative. Accounting for the damages conservatively doubles to triples the price of electricity from coal per kWh generated, making wind, solar, and other forms of nonfossil fuel power generation, along with investments in efficiency and electricity conservation methods, economically competitive. We focus on Appalachia, though coal is mined in other regions of the United States and is burned throughout the world.

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Photoluminescence (PL) quantum efficiency is a key issue in designing successful light-emitting polymer systems. Exciton relaxation is strongly affected by exciton quenching at nonradiative trapping centers and the formation of excimers. These factors reduce the PL quantum yield of light-emitting polymers. In this work, we have systematically investigated the effects of exciton confinement on the PL quantum yield of an oligomer, polymer, and alternating block copolymer (ABC) PPV system. Time-resolved and temperature-dependent luminescence studies have been performed. The ABC design effectively confine photoexcitations within the chromophores, preventing exciton migration and excimer formation. An unusually high (PL) quantum yield (above 90%) in the solid state is reported for the alternating block copolymer PPV, as compared to that of similar to 30% of the polymer and oligomer model compounds. (C) 2000 Elsevier Science S.A. All rights reserved.

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Infrared emission at 1.54 mu m excited optically and electrically from an erbium organic compound tris(acetylacetonato)(1,10-phenanthroline) erbium [Er(acac)(3)(phen)] is observed. The rare-earth complex is dispersed into a polymer matrix of poly(N-vinylcarbazole) (PVK) to fabricate an electroluminescent (EL) device with an ITO/PVK:Er(acac)(3)(phen)/Al:Li/Ag structure, where ITO represents indium-tin-oxide-coated glass. The device shows infrared EL emission at 1.54 mu m, which suggests a simple and cheap method to obtain a light source for 1.54-mu m-wavelength devices in optical communications. (C) 2000 American Institute of Physics. [S0021-8979(00)00301-7].

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We present an online distributed algorithm, the Causation Logging Algorithm (CLA), in which Autonomous Systems (ASes) in the Internet individually report route oscillations/flaps they experience to a central Internet Routing Registry (IRR). The IRR aggregates these reports and may observe what we call causation chains where each node on the chain caused a route flap at the next node along the chain. A chain may also have a causation cycle. The type of an observed causation chain/cycle allows the IRR to infer the underlying policy routing configuration (i.e., the system of economic relationships and constraints on route/path preferences). Our algorithm is based on a formal policy routing model that captures the propagation dynamics of route flaps under arbitrary changes in topology or path preferences. We derive invariant properties of causation chains/cycles for ASes which conform to economic relationships based on the popular Gao-Rexford model. The Gao-Rexford model is known to be safe in the sense that the system always converges to a stable set of paths under static conditions. Our CLA algorithm recovers the type/property of an observed causation chain of an underlying system and determines whether it conforms to the safe economic Gao-Rexford model. Causes for nonconformity can be diagnosed by comparing the properties of the causation chains with those predicted from different variants of the Gao-Rexford model.

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In this paper we introduce a theory of policy routing dynamics based on fundamental axioms of routing update mechanisms. We develop a dynamic policy routing model (DPR) that extends the static formalism of the stable paths problem (introduced by Griffin et al.) with discrete synchronous time. DPR captures the propagation of path changes in any dynamic network irrespective of its time-varying topology. We introduce several novel structures such as causation chains, dispute fences and policy digraphs that model different aspects of routing dynamics and provide insight into how these dynamics manifest in a network. We exercise the practicality of the theoretical foundation provided by DPR with two fundamental problems: routing dynamics minimization and policy conflict detection. The dynamics minimization problem utilizes policy digraphs, that capture the dependencies in routing policies irrespective of underlying topology dynamics, to solve a graph optimization problem. This optimization problem explicitly minimizes the number of routing update messages in a dynamic network by optimally changing the path preferences of a minimal subset of nodes. The conflict detection problem, on the other hand, utilizes a theoretical result of DPR where the root cause of a causation cycle (i.e., cycle of routing update messages) can be precisely inferred as either a transient route flap or a dispute wheel (i.e., policy conflict). Using this result we develop SafetyPulse, a token-based distributed algorithm to detect policy conflicts in a dynamic network. SafetyPulse is privacy preserving, computationally efficient, and provably correct.

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We introduce Active Hidden Models (AHM) that utilize kernel methods traditionally associated with classification. We use AHMs to track deformable objects in video sequences by leveraging kernel projections. We introduce the "subset projection" method which improves the efficiency of our tracking approach by a factor of ten. We successfully tested our method on facial tracking with extreme head movements (including full 180-degree head rotation), facial expressions, and deformable objects. Given a kernel and a set of training observations, we derive unbiased estimates of the accuracy of the AHM tracker. Kernels are generally used in classification methods to make training data linearly separable. We prove that the optimal (minimum variance) tracking kernels are those that make the training observations linearly dependent.

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We introduce the Dynamic Policy Routing (DPR) model that captures the propagation of route updates under arbitrary changes in topology or path preferences. DPR introduces the notion of causation chains where the route flap at one node causes a flap at the next node along the chain. Using DPR, we model the Gao-Rexford (economic) guidelines that guarantee the safety (i.e., convergence) of policy routing. We establish three principles of safe policy routing dynamics. The non-interference principle provides insight into which ASes can directly induce route changes in one another. The single cycle principle and the multi-tiered cycle principle provide insight into how cycles of routing updates can manifest in any network. We develop INTERFERENCEBEAT, a distributed algorithm that propagates a small token along causation chains to check adherence to these principles. To enhance the diagnosis power of INTERFERENCEBEAT, we model four violations of the Gao-Rexford guidelines (e.g., transiting between peers) and characterize the resulting dynamics.

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The cascade that culminates in macrometastases is thought to be mediated by phenotypic plasticity, including epithelial-mesenchymal and mesenchymal-epithelial transitions (EMT and MET). Although there is substantial support for the role of EMT in driving cancer cell invasion and dissemination, much less is known about the importance of MET in the later steps of metastatic colonization. We created novel reporters, which integrate transcriptional and post-transcriptional regulation, to test whether MET is required for metastasis in multiple in vivo cancer models. In a model of carcinosarcoma, metastasis occurred via an MET-dependent pathway; however, in two prostate carcinoma models, metastatic colonization was MET independent. Our results provide evidence for both MET-dependent and MET-independent metastatic pathways.

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This chapter focuses on what the key decision makers in organizations decide after having received information on the current state of the organizational performance. Because of strong attributions to success and failure, it is impossible to predict in advance which concrete actions will occur. We can however find out what kinds of actions are decided upon by means of an organizational learning model that focuses on the hastenings and delays after performance feedback. As an illustration, the responses to performance signals by trainers and club owners in Dutch soccer clubs are analyzed.

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This article has been written with the intention of being able to analyse the contributions of art —theatre, in this case— to the practice of social work. For this purpose, we have chosen to read the social reality in which we intervene through the lens of social constructionism. This helps us to rescue the social and subjective side of art, and, moreover, to recover the depathologization of the subject in professional intervention. Thus, using a practical case taken from work with adolescents in the German FSJ programme, hand-in-hand with a young girl called Anja we trace the developmental and sociological aspects of adolescence in order to later address certain common points of art and psychosocial work. Art will hence be redefined as a transitional object allowing questions to be addressed relating to (self-) perception, attachment, communication and changes in conduct as the ultimate goal of professional action. Lastly, we note the limitations and risks of art-based intervention, in order to conclude with a final synopsis.

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A proportion of Hodgkin lymphoma (HL) cases are causally associated with the Epstein-Barr virus (EBV) but the aetiology of the remaining cases remains obscure. Over the last 3 decades several studies have found an association between HL and measles virus (MV) including a recent cohort study describing the detection of MV antigens in Hodgkin and Reed-Sternberg cells, the tumour cells in HL. In the present study we looked at the relationship between history of MV infection and risk of developing HL in a population-based, case/control study of HL. In addition we used immunohistochemistry and RT-PCR to look for direct evidence of MV in HL biopsies. There was no significant difference in the proportion of cases reporting previous measles compared to controls in the entire data set or when young adults were considered separately. Using a robust immunohistochemical assay for MV infection, we failed to find evidence of MV in biopsies from 97 cases of HL and RT-PCR studies similarly gave negative results. This study therefore provides no evidence that MV is directly involved in the development of HL. However, when age at first reported MV infection was investigated, significant differences emerged with children infected before school-age having higher risk, especially of EBV-ve HL, when compared with children infected at older ages; the interpretation of these latter results is unclear.

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Previous reports have shown that DNA methylation profiles within primary human malignant tissues are altered when these cells are transformed into cancer cell lines. However, it is unclear if similar differences in DNA methylation profiles exist between DNA derived from peripheral blood leukocytes (PBLs) and corresponding Epstein-Barr Virus transformed lymphoblastoid cell lines (LCLs). To assess the utility of LCLs as a resource for methylation studies we have compared DNA methylation profiles in promoter and 5' regions of 318 genes in PBL and LCL sample pairs from patients with type 1 diabetes with or without nephropathy. We identified a total of 27 (similar to 8%) genes that revealed different DNA methylation profiles in PBL compared with LCL-derived DNA samples. In conclusion, although the profiles for most promoter regions were similar between PBL-LCL pairs, our results indicate that LCL-derived DNA may not be suitable for DNA methylation studies at least in diabetic nephropathy.

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Objectives: We sought to replicate the association between the kinesin-like protein 6 (KIF6) Trp719Arg polymorphism (rs20455), and clinical coronary artery disease (CAD).
Background: Recent prospective studies suggest that carriers of the 719Arg allele in KIF6 are at increased risk of clinical CAD compared with noncarriers.
Methods: The KIF6 Trp719Arg polymorphism (rs20455) was genotyped in 19 case-control studies of nonfatal CAD either as part of a genome-wide association study or in a formal attempt to replicate the initial positive reports.
Results: A total of 17,000 cases and 39,369 controls of European descent as well as a modest number of South Asians, African Americans, Hispanics, East Asians, and admixed cases and controls were successfully genotyped. None of the 19 studies demonstrated an increased risk of CAD in carriers of the 719Arg allele compared with noncarriers. Regression analyses and fixed-effects meta-analyses ruled out with high degree of confidence an increase of <2% in the risk of CAD among European 719Arg carriers. We also observed no increase in the risk of CAD among 719Arg carriers in the subset of Europeans with early-onset disease (younger than 50 years of age for men and younger than 60 years of age for women) compared with similarly aged controls as well as all non-European subgroups.
Conclusions: The KIF6 Trp719Arg polymorphism was not associated with the risk of clinical CAD in this large replication study.