A tabular source approach to modelling and simulating device and circuit noise in the time domain

Simulation of device and circuit noise at low frequencies is often carried out as part of a small‐signal ac analysis. Moreover, circuit simulators with rf analysis capabilities usually specify circuit performance in terms of S parameters and model high‐frequency noise in terms of noise waves and correlation matrices. It is also unusual to find circuit simulators that extend noise simulation to the time domain. This is particularly true for software packages developed from SPICE 2g6 or 3f5. This paper introduces a simple tabular noise source technique, which adds time‐domain noise to semiconductor device models and integrated circuit macromodels. The proposed technique is suitable for use with any general purpose circuit simulator. To demonstrate the power of the suggested approach the text describes time‐domain noise extensions to the SPICE diode, BJT, JFET, MOSFET and MESFET models. These noise extensions have been implemented and tested with the ‘Quite universal circuit simulator’ (Qucs). Copyright © 2011 John Wiley & Sons, Ltd.     

Simulation of the efficiency of hydrogen recombiners as safety devices

Passive auto-catalytic recombiners (PARs) may be used in the future as safety devices inside confined areas for the removal of accidentally released hydrogen. In the presented study, it was investigated whether a PAR designed for hydrogen removal inside an NPP containment would principally work inside a typical surrounding of hydrogen or fuel cell applications. For this purpose, a hydrogen release scenario inside a garage – based on experiments performed by CEA in the GARAGE facility (France) – has been simulated with and without PAR installation. For modeling the operational behavior of the PAR, the in-house code REKO-DIREKT was implemented in the CFD code ANSYS-CFX. The study was performed in three steps: First, a helium release scenario was simulated and validated against experimental data. Second, helium was replaced by hydrogen in the simulation. This step served as a reference case for the unmitigated scenario. Finally, the numerical garage setup was enhanced with a commercial PAR model. The study shows that the PAR works efficiently by removing hydrogen and promoting mixing inside the garage. The hot exhaust plume promotes the formation of a thermal stratification that pushes the initial hydrogen rich gas downwards and in direction of the PAR inlet. The paper describes the code implementation and simulation results.     

声波测井网络理论Ⅰ:声源信号的产生方法和数值模拟

利用薄球壳压电换能器的等效电路可以解析地确定在薄球壳压电换能器被电激励信号激发过程中， 周围耦合介质对它的作用力和它的瞬态响应，给出了用驱动电压信号激励换能器使其辐射出马鞍组特殊测井需要的声源信号，由于薄球壳换能器在所有的方向上均匀地向外辐射声波信号，因此在声波测井的正演研究和数值模拟中，可以把它等效为一个点源。     

Polyamine spider toxins and mammalian N-methyl-D-aspartate receptors. Structural basis for channel blocking and binding of argiotoxin636

Recombinant N-methyl-D-aspartate receptors composed of NR1/NR2A subunits were expressed in Xenopus oocytes to analyse the voltage-dependent and use-dependent channel blocking activity of argiotoxin636. Functional assays demonstrate that the toxin competes with other open channel blockers such as Mg2+ and MK-801. Direct binding or competition assays using radiolabeled ligands and isolated rat brain membranes, in contrast, reveal no specific binding or yield binding constants which differ by orders of magnitude from the IC50 values of the functional assays. One explanation is that argiotoxin636 does not bind with high affinity to the inhibitory site in the N-methyl-D-aspartate-receptor channel under in vitro conditions when membranes are depolarised. The structure of argiotoxin636 was investigated by NMR spectroscopy. In solution the positively charged argiotoxin636 acquires an extended conformation and its dimensions might allow permeation deep into the channel. In the absence of direct structural information on the channel protein, the detailed analysis of blockade in conjunction with structural information, as provided here, may be of aid in the deduction of structural features of glutamate-receptor channel ion pores.     

Beta 1-adrenoceptor subtype selective antagonism of esmolol and its major metabolite in vitro and in man. Investigations using tricresylphosphate as red blood cell carboxylesterase inhibitor

Esmolol (CAS 103598-03-4, ASL-8052, Brevibloc) is an ultrashort acting beta-adrenoceptor antagonist which is rapidly hydrolyzed by a red blood cell esterase. In order to investigate the affinity profile of esmolol and its acid metabolite at beta-adrenoceptor subtypes in plasma and in whole blood in radioligand binding studies a potent esterase inhibitor was needed to prevent hydrolysis of esmolol and--in contrast to sodium fluoride--without influencing binding of the drugs at the receptor site. Tricresylphosphate was found to be a potent inhibitor of hydrolysis of esmolol which did not affect the parameters of radioligand binding. During an incubation time of 15 min at 25 degrees C in whole blood no significant metabolism of esmolol took place whereas without addition of inhibitor about 20% were inactivated. Thus, for the first time exact determinations of plasma concentrations of esmolol by ligand binding studies could be carried out. In vitro in radioligand binding studies esmolol had a 34 fold higher affinity for beta 1-adrenoceptors than for beta 2-adrenoceptors. Its acid metabolite had a very low and nonselective affinity for both adrenoceptor subtypes: Compared with esmolol it was 400fold less potent at beta 1-adrenoceptors. When plasma concentrations of esmolol and its metabolite after i.v. administration of esmolol to healthy volunteers (3000 micrograms/kg as a bolus and consecutively 500 micrograms/kg/min for 70 min) were determined in parallel by a beta 1-selective radioreceptor assay and an HPLC-method the following conclusions could be drawn from the direct correlation between the respective results: 1. (ABSTRACT TRUNCATED AT 250 WORDS)     

Genomic analysis of the F subtypes of human complement factor B

Factor B of human complement is encoded within the Major Histocompatibility Complex (MHC) and is polymorphic, with up to 30 alleles defined by electrophoretic mobility. One of the most common alleles, BF*F, is subdivided into the FA and FB subtypes, which differ at the gene level by non-synonymous base substitutions in the seventh codon. We have found at this position a new restriction site polymorphism, as a Bsl I site absent from the FB allele. Using this restriction polymorphism, we have developed a method for BF F subtype determination, based on amplification by polymerase chain reaction of the 5' end of the BF gene, and digestion with Bsl I. This new method has been applied to a panel of 29 selected BF F individuals. A single strand DNA conformation analysis of the same region of the gene allowed us to confirm the above DNA-based BF F subtyping. During this study, two BF*F1 alleles showed discrepancies between protein and DNA typing, which were confirmed by our sequencing data. These were identical, in the 5' region, to BF*S and BF*FB genes, respectively. In a comparison with two protein subtyping methods, identical results were found for only one third of the selected samples. The conflicting results may arise, in part, from previously undescribed molecular heterogeneity within BF F subtypes, or from the presence of a null allele. Our new method allows BF*F subtyping to be used with confidence in the definition of disease-associated MHC haplotypes.