Identification of Slow States at the SiO2/SiC Interface through Sub-Bandgap Illumination

We show that it is possible to obtain information relating to deep level interface traps, or so called ‘slow states’, by using the photo-CV characterisation method. Sub-bandgap illumination has been chosen in order to avoid band-to-band excitation for the creation of minority carriers. This enables information to be extracted from trapping states at the SiO2/SiC interface that are energetically deep within the band gap. Empirical observations of deep level trapping states with life times in the order of tens of hours are reported and the interface trap density as a function of energy has been extracted using the Terman method. Characterisation of these interface states will aid the development of new fabrication processes, with the aim of reducing the interface trap density to the same level as that of the SiO2/Si interface and facilitating the production of higher quality SiC based devices

Domain Walls in Two-Component Dynamical Lattices

We introduce domain-wall (DW) states in the bimodal discrete nonlinear Schr{\"{o}}dinger equation, in which the modes are coupled by cross phase modulation (XPM). By means of continuation from various initial patterns taken in the anti-continuum (AC) limit, we find a number of different solutions of the DW type, for which different stability scenarios are identified. In the case of strong XPM coupling, DW configurations contain a single mode at each end of the chain. The most fundamental solution of this type is found to be always stable. Another solution, which is generated by a different AC pattern, demonstrates behavior which is unusual for nonlinear dynamical lattices: it is unstable for small values of the coupling constant $C$ (which measures the ratio of the nonlinearity and coupling lengths), and becomes stable at larger $C$. Stable bound states of DWs are also found. DW configurations generated by more sophisticated AC patterns are identified as well, but they are either completely unstable, or are stable only at small values of $C$. In the case of weak XPM, a natural DW solution is the one which contains a combination of both polarizations, with the phase difference between them 0 and $\pi$ at the opposite ends of the lattice. This solution is unstable at all values of $C$, but the instability is very weak for large $C$, indicating stabilization as the continuum limit is approached. The stability of DWs is also verified by direct simulations, and the evolution of unstable DWs is simulated too; in particular, it is found that, in the weak-XPM system, the instability may give rise to a moving DW.Comment: 14 pages, 14 figures, Phys. Rev. E (in press

Homogenized dynamics of stochastic partial differential equations with dynamical boundary conditions

A microscopic heterogeneous system under random influence is considered. The randomness enters the system at physical boundary of small scale obstacles as well as at the interior of the physical medium. This system is modeled by a stochastic partial differential equation defined on a domain perforated with small holes (obstacles or heterogeneities), together with random dynamical boundary conditions on the boundaries of these small holes. A homogenized macroscopic model for this microscopic heterogeneous stochastic system is derived. This homogenized effective model is a new stochastic partial differential equation defined on a unified domain without small holes, with static boundary condition only. In fact, the random dynamical boundary conditions are homogenized out, but the impact of random forces on the small holes' boundaries is quantified as an extra stochastic term in the homogenized stochastic partial differential equation. Moreover, the validity of the homogenized model is justified by showing that the solutions of the microscopic model converge to those of the effective macroscopic model in probability distribution, as the size of small holes diminishes to zero.Comment: Communications in Mathematical Physics, to appear, 200

Twenty-three unsolved problems in hydrology (UPH) – a community perspective

This paper is the outcome of a community initiative to identify major unsolved scientific problems in hydrology motivated by a need for stronger harmonisation of research efforts. The procedure involved a public consultation through on-line media, followed by two workshops through which a large number of potential science questions were collated, prioritised, and synthesised. In spite of the diversity of the participants (230 scientists in total), the process revealed much about community priorities and the state of our science: a preference for continuity in research questions rather than radical departures or redirections from past and current work. Questions remain focussed on process-based understanding of hydrological variability and causality at all space and time scales. Increased attention to environmental change drives a new emphasis on understanding how change propagates across interfaces within the hydrological system and across disciplinary boundaries. In particular, the expansion of the human footprint raises a new set of questions related to human interactions with nature and water cycle feedbacks in the context of complex water management problems. We hope that this reflection and synthesis of the 23 unsolved problems in hydrology will help guide research efforts for some years to come

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies