Development of the Magnetic Excitations of Charge-Stripe Ordered La(2-x)Sr(x)NiO(4) on Doping Towards Checkerboard Charge Order

The magnetic excitation spectrums of charge stripe ordered La(2-x)Sr(x)NiO(4) x = 0.45 and x = 0.4 were studied by inelastic neutron scattering. We found the magnetic excitation spectrum of x = 0.45 from the ordered Ni^2+ S = 1 spins to match that of checkerboard charge ordered La(1.5)Sr(0.5)NiO(4). The distinctive asymmetry in the magnetic excitations above 40 meV was observed for both doping levels, but an additional ferromagnetic mode was observed in x = 0.45 and not in the x = 0.4. We discuss the origin of crossover in the excitation spectrum between x = 0.45 and x = 0.4 with respect to discommensurations in the charge stripe structure.Comment: 4 Figures. To be appear in the J. Kor. Phys. Soc. as a proceedings paper from the ICM 2012 conferenc

Investigation of the collapse of the skewness and kurtosis exhibited in atmospheric dispersion data

This paper studies the collapse of the estimators for skewness and kurtosis of concentration onto a near universal curve. This phenomenon is observed for data taken from atmospheric dispersion experiments under a variety of different conditions. By means of careful investigation of the high concentration tails, modelled by means of the generalized Pareto distribution, and the fundamental physics of the problem, a set of envelope curves encompassing the data will be established. The implications of these results for modelling the probability density function of concentration are discussed

Comments on the properties and uses of atmospheric dispersion datasets

Great recent improvements in the quality and quantity of atmospheric dispersion datasets have highlighted the crucial importance of concentration fluctuations. However, this has inevitably been accompanied by the realisation that estimating the properties of concentration fluctuations accurately involves new, difficult, but interesting, research problems. Some of these problems are discussed and illustrated. The paper concludes with some recommendations about how research funding agencies (such as governments, regulatory authorities and industry) should change their present strategy in response to new knowledge

Cognitive decline heralds onset of symptomatic inherited prion disease

The clinical effectiveness of any disease-modifying treatment for prion disease, as for other neurodegenerative disorders, will depend on early treatment before damage to neural tissue is irrevocable. Thus, there is a need to identify markers that predict disease onset in healthy at-risk individuals. Whilst imaging and neurophysiological biomarkers have shown limited use in this regard, we recently reported progressive neurophysiological changes in individuals with the inherited prion disease mutation P102L. We have also previously demonstrated a signature pattern of fronto-parietal dysfunction in mild prion disease. Here we address whether these cognitive features anticipate the onset of symptoms in a unique sample of patients with inherited prion disease. In the cross-sectional analysis, we analysed the performance of patients at three time points in the course of disease onset: prior to symptoms (n = 27), onset of subjective symptoms without positive clinical findings (n = 8) and symptomatic with positive clinical findings (n = 24). In the longitudinal analysis, we analysed data from 24 patients who were presymptomatic at the time of recruitment and were followed up over a period of up to 17 years, of whom 16 remained healthy and eight converted to become symptomatic. In the cross-sectional analysis, the key finding was that, relative to a group of 25 healthy non-gene carrier controls, patients with subjective symptoms but without positive clinical findings were impaired on a smaller but similar set of tests (Trail Making Test part A, Stroop test, Performance IQ, gesture repetition, figure recall) to those previously found to be impaired in mild prion disease. In the longitudinal analysis, Trail Making Test parts A and B, Stroop test and Performance IQ scores significantly discriminated between patients who remained presymptomatic and those who converted, even before the converters reached criteria for formal diagnosis. Notably, performance on the Stroop test significantly discriminated between presymptomatic patients and converters before the onset of clinical symptoms [area under the curve = 0.83 (95% confidence interval, 0.62–1.00), P = 0.009]. Thus, we report here, for the first time, neuropsychological abnormalities in healthy patients prior to either symptom onset or clinical diagnosis of inherited prion disease. This constitutes an important component of an evolving profile of clinical and biomarker abnormalities in this crucial group for preventive medicine

Cognitive decline heralds onset of symptomatic inherited prion disease

The clinical effectiveness of any disease-modifying treatment for prion disease, as for other neurodegenerative disorders, will depend on early treatment before damage to neural tissue is irrevocable. Thus, there is a need to identify markers which predict disease onset in healthy at-risk individuals. Whilst imaging and neurophysiological biomarkers have shown limited use in this regard, we recently reported progressive neurophysiological changes in healthy people with the inherited prion disease mutation P102L (Rudge et al, Brain 2019). We have also previously demonstrated a signature pattern of fronto-parietal dysfunction in mild prion disease (Caine et al., 2015; 2018). Here we address whether these cognitive features anticipate the onset of symptoms in a unique sample of patients with inherited prion disease. In the cross-sectional analysis, we analysed the performance of patients at three time points in the course of disease onset: prior to symptoms (n = 27), onset of subjective symptoms without positive clinical findings (n = 8) and symptomatic with positive clinical findings (n = 24). In the longitudinal analysis, we analysed data from twenty four patients who were presymptomatic at the time of recruitment and were followed up over a period of up to seventeen years, of whom sixteen remained healthy and eight converted to become symptomatic. In the cross-sectional analysis, the key finding was that, relative to a group of 25 healthy non-gene carrier controls, patients with subjective symptoms but without positive clinical findings were impaired on a smaller but very similar set of tests (Trail Making Test part A, Stroop Test, Performance IQ, gesture repetition, figure recall) to those previously found to be impaired in mild prion disease (Caine et al., 2015; 2018). In the longitudinal analysis, Trail Making Test parts A and B, Stroop test and Performance IQ scores significantly discriminated between patients who remained presymptomatic and those who converted, even before the converters reached criteria for formal diagnosis. Notably, performance on the Stroop test significantly discriminated between presymptomatic patients and converters before the onset of clinical symptoms (AUC = .83 (95% CI, 0.62-1.00), p =.009). Thus, we report here, for the first time, neuropsychological abnormalities in healthy patients prior to either symptom onset or clinical diagnosis of IPD. This constitutes an important component of an evolving profile of clinical and biomarker abnormalities in this crucial group for preventive medicine

Magnetic excitations of the charge stripe electrons below half doping in La2−xSrxNiO4 (x = 0.45, 0.4)

The low energy magnetic excitation spectrum of charge stripe ordered La2−xSrxNiO4, x = 0.4 and x = 0.45 were studied by neutron scattering. Two excitation modes are observed in both materials, one from the ordered magnetic moments, and a second mode consistent with pseudo-onedimensional antiferromagnetic excitations of the charge stripe electrons (q-1D). The dispersion of the q-1D excitation follows the same relation as in x = 1/3 composition, with even spectral weight in the two counter-propagating branches of the x = 0.4, however in the x = 0.45 only one dispersion branch has any measurable spectral weight. The evolution of the q-1D excitations on doping to the checkerboard charge ordered phase is discussed

Being Sympathetic to Bad-History Wrongdoers

For many philosophers, bad-history wrongdoers are primarily interesting because of what their cases might tell us about the interaction of moral responsibility and history. However, philosophers focusing on blameworthiness have overlooked important questions about blame itself. These bad-history cases are complicated because blame and sympathy are both fitting. When we are careful to consider the rich natures of those two reactions, we see that they conflict in several important ways. We should see bad-history cases as cases about whether and how we should blame, rather than as cases giving us ready insight into the nature of moral responsibility