Harmonic balance surrogate-based immunity modeling of a nonlinear analog circuit

A novel harmonic balance surrogate-based technique to create fast and accurate behavioral models predicting, in the early design stage, the performance of nonlinear analog devices during immunity tests is presented. The obtained immunity model hides the real netlist, reduces the simulation time, and avoids expensive and time-consuming measurements after tape-out, while still providing high accuracy. The model can easily be integrated into a circuit simulator together with additional subcircuits, e.g., board and package models, as such allowing to efficiently reproduce complete immunity test setups during the early design stage and without disclosing any intellectual property. The novel method is validated by means of application to an industrial case study, being an automotive voltage regulator, clearly showing the technique's capabilities and practical advantages

Effects of Heavy-Ion Irradiation on Microstructure of V-4Cr-4Ti Alloy at Moderate Temperatures

V-4Cr-4Ti is promising for first-wall and structural applications in magnetic fusion reactors. Fast neutron sources were used to evaluate postirradiation properties of fusion candidate materials, but FFTF and EBR-II have been shutdown. Under these circumstances, heavy-ion irradiation is an attractive alternative. We used 3-MeV V{sup +} and 4.5-MeV Ni{sup 2+} ions to investigate effects of irradiation on microstructure of V-4Cr-4Ti at 200-420 C. This paper report results of ion irradiation experiments and compare with fast-neutron irradiation data. From TEM, the dominant feature of postirradiation microstructure was a high density of dislocation loops and point- defect clusters. Density and defect size depend on irradiation dose and temperature. Precipitates and voids/bubbles were not observed, even in specimens simultaneous injected with he and exposed to heavy ions. Increased transport of point defects to internal interfaces was observed, as manifested by defect denuded zones along grain boundaries. Defect denuded zones along grain boundaries could lead to segregation of impurities and solutes and formation of precipitates on grain boundaries

Antimony substituted lanthanum orthoniobate proton conductor - Structure and electronic properties

X‐ray and neutron diffraction have been utilized to analyze the crystalline and electronic structure of lanthanum orthoniobate substituted by antimony. Using X‐ray absorption spectroscopy and photoelectron spectroscopy, changes in the electronic structure of the material upon substitution have been analyzed. The structural transition temperature between fergusonite and scheelite phases for 30 mol% antimony substitution was found to be 15°C. Based on the neutron data, the oxygen nonstoichiometry was found to be relatively low. Moreover no influence on the position of the valence band maximum was observed. The influence of the protonation on the electronic structure of constituent oxides has been studied. Absorption data show that the incorporation of protonic defects into the lanthanum orthoniobate structure leads to changes in lanthanum electronic structure and a decrease in the density of unoccupied electronic states

Conformance relations and hyperproperties for doping detection in time and space

We present a novel and generalised notion of doping cleanness for cyber-physical systems that allows for perturbing the inputs and observing the perturbed outputs both in the time- and value-domains. We instantiate our definition using existing notions of conformance for cyber-physical systems. As a formal basis for monitoring conformance-based cleanness, we develop the temporal logic HyperSTL*, an extension of Signal Temporal Logics with trace quantifiers and a freeze operator. We show that our generalised definitions are essential in a data-driven method for doping detection and apply our definitions to a case study concerning diesel emission tests

Why Are Male Social Relationships Complex in the Doubtful Sound Bottlenose Dolphin Population?

Copyright 2008 Elsevier B.V., All rights reserved.Peer reviewedPublisher PD

Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase

Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene mutations that lead to ribosomal insufficiency. DBA is characterized by anemia, congenital anomalies, and cancer predisposition. Treatment for DBA is associated with significant morbidity. Here, we report the identification of Nemo-like kinase (NLK) as a potential target for DBA therapy. To identify new DBA targets, we screen for small molecules that increase erythroid expansion in mouse models of DBA. This screen identified a compound that inhibits NLK. Chemical and genetic inhibition of NLK increases erythroid expansion in mouse and human progenitors, including bone marrow cells from DBA patients. In DBA models and patient samples, aberrant NLK activation is initiated at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differentiation and is not observed in non-erythroid hematopoietic lineages or healthy erythroblasts. We propose that NLK mediates aberrant erythropoiesis in DBA and is a potential target for therapy

Oink: an Implementation and Evaluation of Modern Parity Game Solvers

Parity games have important practical applications in formal verification and synthesis, especially to solve the model-checking problem of the modal mu-calculus. They are also interesting from the theory perspective, as they are widely believed to admit a polynomial solution, but so far no such algorithm is known. In recent years, a number of new algorithms and improvements to existing algorithms have been proposed. We implement a new and easy to extend tool Oink, which is a high-performance implementation of modern parity game algorithms. We further present a comprehensive empirical evaluation of modern parity game algorithms and solvers, both on real world benchmarks and randomly generated games. Our experiments show that our new tool Oink outperforms the current state-of-the-art.Comment: Accepted at TACAS 201

Altered translation of GATA1 in Diamond-Blackfan anemia

Ribosomal protein haploinsufficiency occurs in diverse human diseases including Diamond-Blackfan anemia (DBA),1,2 congenital asplenia,3 and T-cell leukemia.4 Yet how mutations in such ubiquitously expressed proteins result in cell-type and tissue specific defects remains a mystery.5 Here, we show that GATA1 mutations that reduce full-length protein levels of this critical hematopoietic transcription factor can cause DBA in rare instances. We show that ribosomal protein haploinsufficiency, the more common cause of DBA, can similarly reduce translation of GATA1 mRNA - a phenomenon that appears to result from this mRNA having a higher threshold for initiation of translation. In primary hematopoietic cells from patients with RPS19 mutations, a transcriptional signature of GATA1 target genes is globally and specifically reduced, confirming that the activity, but not the mRNA level, of GATA1 is reduced in DBA patients with ribosomal protein mutations. The defective hematopoiesis observed in DBA patients with ribosomal protein haploinsufficiency can be at least partially overcome by increasing GATA1 protein levels. Our results provide a paradigm by which selective defects in translation due to mutations in ubiquitous ribosomal proteins can result in human disease

Altered translation of GATA1 in Diamond-Blackfan anemia

Ribosomal protein haploinsufficiency occurs in diverse human diseases including Diamond-Blackfan anemia (DBA)[superscript 1, 2], congenital asplenia[superscript 3] and T cell leukemia[superscript 4]. Yet, how mutations in genes encoding ubiquitously expressed proteins such as these result in cell-type– and tissue-specific defects remains unknown[superscript 5]. Here, we identify mutations in GATA1, encoding the critical hematopoietic transcription factor GATA-binding protein-1, that reduce levels of full-length GATA1 protein and cause DBA in rare instances. We show that ribosomal protein haploinsufficiency, the more common cause of DBA, can lead to decreased GATA1 mRNA translation, possibly resulting from a higher threshold for initiation of translation of this mRNA in comparison with other mRNAs. In primary hematopoietic cells from patients with mutations in RPS19, encoding ribosomal protein S19, the amplitude of a transcriptional signature of GATA1 target genes was globally and specifically reduced, indicating that the activity, but not the mRNA level, of GATA1 is decreased in patients with DBA associated with mutations affecting ribosomal proteins. Moreover, the defective hematopoiesis observed in patients with DBA associated with ribosomal protein haploinsufficiency could be partially overcome by increasing GATA1 protein levels. Our results provide a paradigm by which selective defects in translation due to mutations affecting ubiquitous ribosomal proteins can result in human disease.National Institutes of Health (U.S.) (Grant P01 HL32262)National Institutes of Health (U.S.) (Grant U54 HG003067-09