Improved plaque materials for aerospace nickel-cadmium cells

Improved cadmium electrode substrates with precisely controlled microstructures for possible use in aerospace nickel-cadmium cells were prepared. The preparative technique was a powder metallurgical process in which a fugitive pore-former and a nickel powder were blended, then isostatically compacted, and subsequently sintered. Cadmium electrodes prepared from such substrates were cycle tested using an accelerated tortuous test regime. It was discovered that plaques of 60% or 80% porosity prepared with a 25 micron pore-former were better than state-of-the-art electrodes in terms of efficienty and/or mechanical strength. The 60% structures were particularly outstanding in this respect in that they had efficiencies only 5-10 percentage points lower than state-of-the-art electrodes and vastly superior mechanical properties. This added strength was observed to eliminate cracking and physical degradation of the electrodes during processing and cycling. The cadmium electrodes prepared from the 80% porous substrates proved to be the best electrodes made during the course of the work from the point of view of highest efficiency. Three-point bend tests were used to measure mechanical properties of the plaques produced and also as a general characterization tool. In addition, the BET surface areas of selected specimens was determined. The SEM was used for judging microscopic uniformity and quantitatively determining the induced pore size and various other fine structures in the substrates. The technique of X-ray radiography was used to follow the bulk uniformity of the substrates at various stages of their processing

Tests of Diet and Insulin-like Peptides on the Duration of the 5th Instar of Male Lubber Grasshoppers

Consuming fewer calories while maintaining adequate nutrition (i.e. calorie restriction), even if that diet is started late in life, rapidly increases longevity by slowing the aging process (Mair et al. 2003). The mechanisms underlying rapidly reduced mortality rate in response to late-onset calorie restriction are largely unknown. Calorie restriction is associated with lower insulin-like peptides (ILP) levels in many organisms (Tater et al. 2003). We have shown that calorie restriction throughout adulthood, and late-onset calorie restriction, increases longevity in female grasshoppers (Wells et al. 2005; Hatle et al. 2006). The exact role of ILP in the enhanced longevity due to late-onset calorie restriction is unclear. Consequently, there is a need for experiments in which insulin signaling is manipulated only late in life.Insulin is the hormone secreted by the pancreas of vertebrates that aids in the membrane transport of glucose from the blood into the body cells (Marieb 2005). More generally, insulin directs the absorptive state. Typically, insulin levels increase upon feeding, at which time energy is available for cells to grow. In this role, insulin acts as a growth regulator and signals cells to divide. In lower organisms like insects, ILP are present and appear to act primarily as growth regulators, with little role in glucose metabolism (Ebberink et al. 1989). Previous research on fruit flies has shown that removal of insulin-producing cells causes developmental delays and growth retardation (Rulifson et al. 2002). Hence, we sought to develop an experimental system to test the role of insulin signaling in calorie restriction. The duration of the 5th instar (the stage prior to adulthood) is affected by diet level in juvenile male lubber grasshoppers (Hatle et al. 2003). Developmental events that are affected by calorie intake likely are affected by insulin signaling. To determine whether maturation to adult molt in grasshoppers can be affected by insulin signaling, we injected grasshoppers with an antibody to human insulin (anti-insulin) and measured developmental timing

Sub-doppler two-photon spectrum of asymmetric rotor molecules

The Doppler-free two-photon excitation spectrum of the qqQ branch of the 1410 vibrational band of the S1(1B2u) ← S0(1A1g) transition of benzene-d1 has been recorded using a cw single-mode dye laser coupled to an external concentric resonator. The spectrum has been analysed using a non-rigid Watson Hamiltonian. More than 200 lines with J up to 20 have been assigned and the rotational constants which best reproduce the spectrum are A1v = 0.181435, B1v = 0.169990, C1v = 0.089055 cm−1. The Ka = odd lines of the qqQ5(J) subbranch show small and quite regular perturbations of 60 ± 5 MHz which are probably due to a coupling to another vibrational state of the S1 manifold

Nur77 controls tolerance induction, terminal differentiation, and effector functions in semi-invariant natural killer T cells

Semi-invariant natural killer T (iNKT) cells are self-reactive lymphocytes, yet how this lineage attains self-tolerance remains unknown. iNKT cells constitutively express high levels of Nr4a1-encoded Nur77, a transcription factor that integrates signal strength downstream of the T cell receptor (TCR) within activated thymocytes and peripheral T cells. The function of Nur77 in iNKT cells is unknown. Here we report that sustained Nur77 overexpression (Nur77^(tg)) in mouse thymocytes abrogates iNKT cell development. Introgression of a rearranged Vα14-Jα18 TCR-α chain gene into the Nur77^(tg) (Nur77^(tg);Vα14^(tg)) mouse rescued iNKT cell development up to the early precursor stage, stage 0. iNKT cells in bone marrow chimeras that reconstituted thymic cellularity developed beyond stage 0 precursors and yielded IL-4–producing NKT2 cell subset but not IFN-γ–producing NKT1 cell subset. Nonetheless, the developing thymic iNKT cells that emerged in these chimeras expressed the exhaustion marker PD1 and responded poorly to a strong glycolipid agonist. Thus, Nur77 integrates signals emanating from the TCR to control thymic iNKT cell tolerance induction, terminal differentiation, and effector functions

Nur77 controls tolerance induction, terminal differentiation, and effector functions in semi-invariant natural killer T cells

Semi-invariant natural killer T (iNKT) cells are self-reactive lymphocytes, yet how this lineage attains self-tolerance remains unknown. iNKT cells constitutively express high levels of Nr4a1-encoded Nur77, a transcription factor that integrates signal strength downstream of the T cell receptor (TCR) within activated thymocytes and peripheral T cells. The function of Nur77 in iNKT cells is unknown. Here we report that sustained Nur77 overexpression (Nur77^(tg)) in mouse thymocytes abrogates iNKT cell development. Introgression of a rearranged Vα14-Jα18 TCR-α chain gene into the Nur77^(tg) (Nur77^(tg);Vα14^(tg)) mouse rescued iNKT cell development up to the early precursor stage, stage 0. iNKT cells in bone marrow chimeras that reconstituted thymic cellularity developed beyond stage 0 precursors and yielded IL-4–producing NKT2 cell subset but not IFN-γ–producing NKT1 cell subset. Nonetheless, the developing thymic iNKT cells that emerged in these chimeras expressed the exhaustion marker PD1 and responded poorly to a strong glycolipid agonist. Thus, Nur77 integrates signals emanating from the TCR to control thymic iNKT cell tolerance induction, terminal differentiation, and effector functions

On Quantum State Observability and Measurement

We consider the problem of determining the state of a quantum system given one or more readings of the expectation value of an observable. The system is assumed to be a finite dimensional quantum control system for which we can influence the dynamics by generating all the unitary evolutions in a Lie group. We investigate to what extent, by an appropriate sequence of evolutions and measurements, we can obtain information on the initial state of the system. We present a system theoretic viewpoint of this problem in that we study the {\it observability} of the system. In this context, we characterize the equivalence classes of indistinguishable states and propose algorithms for state identification

Scope for Credit Risk Diversification

This paper considers a simple model of credit risk and derives the limit distribution of losses under different assumptions regarding the structure of systematic risk and the nature of exposure or firm heterogeneity. We derive fat-tailed correlated loss distributions arising from Gaussian risk factors and explore the potential for risk diversification. Where possible the results are generalised to non-Gaussian distributions. The theoretical results indicate that if the firm parameters are heterogeneous but come from a common distribution, for sufficiently large portfolios there is no scope for further risk reduction through active portfolio management. However, if the firm parameters come from different distributions, then further risk reduction is possible by changing the portfolio weights. In either case, neglecting parameter heterogeneity can lead to underestimation of expected losses. But, once expected losses are controlled for, neglecting parameter heterogeneity can lead to overestimation of risk, whether measured by unexpected loss or value-at-risk

Bayesian estimation of incomplete data using conditionally specified priors

In this paper, a class of conjugate prior for estimating incomplete count data based on a broad class of conjugate prior distributions is presented. The new class of prior distributions arises from a conditional perspective, making use of the conditional specification methodology and can be considered as the generalisation of the form of prior distributions that have been used previously in the estimation of in- complete count data well. Finally, some examples of simulated and real data are given

The Role of Industry, Geography and Firm Heterogeneity in Credit Risk Diversification

In theory the potential for credit risk diversification for banks could be substantial. Portfolio diversification is driven broadly by two characteristics: the degree to which systematic risk factors are correlated with each other and the degree of dependence individual firms have to the different types of risk factors. We propose a model for exploring these dimensions of credit risk diversification: across industry sectors and across different countries or regions. We find that full firm-level parameter heterogeneity matters a great deal for capturing differences in simulated credit loss distributions. Imposing homogeneity results in overly skewed and fat-tailed loss distributions. These differences become more pronounced in the presence of systematic risk factor shocks: increased parameter heterogeneity greatly reduces shock sensitivity. Allowing for regional parameter heterogeneity seems to better approximate the loss distributions generated by the fully heterogeneous model than allowing just for industry heterogeneity. The regional model also exhibits less shock sensitivity