On the practicality of time-optimal two-qubit Hamiltonian simulation

What is the time-optimal way of using a set of control Hamiltonians to obtain a desired interaction? Vidal, Hammerer and Cirac [Phys. Rev. Lett. 88 (2002) 237902] have obtained a set of powerful results characterizing the time-optimal simulation of a two-qubit quantum gate using a fixed interaction Hamiltonian and fast local control over the individual qubits. How practically useful are these results? We prove that there are two-qubit Hamiltonians such that time-optimal simulation requires infinitely many steps of evolution, each infinitesimally small, and thus is physically impractical. A procedure is given to determine which two-qubit Hamiltonians have this property, and we show that almost all Hamiltonians do. Finally, we determine some bounds on the penalty that must be paid in the simulation time if the number of steps is fixed at a finite number, and show that the cost in simulation time is not too great.Comment: 9 pages, 2 figure

On the electromagnetic inverse scattering problem

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46179/1/205_2004_Article_BF00282681.pd

Analytical and finite element prediction of Lamb wave scattering at delaminations in quasi-isotropic composite laminates

This paper presents a theoretical and finite element (FE) investigation of the scattering characteristics of the fundamental anti-symmetric (A0) Lamb wave at delaminations in a quasi-isotropic (QI) composite laminate. Analytical models based on the Mindlin plate theory and Born approximation are presented to predict the A0 Lamb wave scattering at a delamination, which is modelled as an inhomogeneity, in an equivalent isotropic model of the QI composite laminate. The results are compared with FE predictions, in which the delamination is modelled as a volume split. The equivalent isotropic model and QI composite laminate are used to investigate the feasibility of the common theoretical approach of modelling the delamination as the inhomogeneity. A good correlation is observed between the theoretical solutions and FE results in the forward scattering amplitudes, but there exists a larger discrepancy in the backward scattering amplitudes. The FE results also show that the fibre direction of the outer laminae has a pronounced influence on the forward and backward scattering amplitudes, which is not predicted by the analytical models.C.T. Ng, M. Veidt, L.R.F. Rose, C.H. Wan

An Observational Overview of Solar Flares

We present an overview of solar flares and associated phenomena, drawing upon a wide range of observational data primarily from the RHESSI era. Following an introductory discussion and overview of the status of observational capabilities, the article is split into topical sections which deal with different areas of flare phenomena (footpoints and ribbons, coronal sources, relationship to coronal mass ejections) and their interconnections. We also discuss flare soft X-ray spectroscopy and the energetics of the process. The emphasis is to describe the observations from multiple points of view, while bearing in mind the models that link them to each other and to theory. The present theoretical and observational understanding of solar flares is far from complete, so we conclude with a brief discussion of models, and a list of missing but important observations.Comment: This is an article for a monograph on the physics of solar flares, inspired by RHESSI observations. The individual articles are to appear in Space Science Reviews (2011

The Marine Microbial Eukaryote Transcriptome Sequencing Project (MMETSP): Illuminating the Functional Diversity of Eukaryotic Life in the Oceans through Transcriptome Sequencing

Microbial ecology is plagued by problems of an abstract nature. Cell sizes are so small and population sizes so large that both are virtually incomprehensible. Niches are so far from our everyday experience as to make their very definition elusive. Organisms that may be abundant and critical to our survival are little understood, seldom described and/or cultured, and sometimes yet to be even seen. One way to confront these problems is to use data of an even more abstract nature: molecular sequence data. Massive environmental nucleic acid sequencing, such as metagenomics or metatranscriptomics, promises functional analysis of microbial communities as a whole, without prior knowledge of which organisms are in the environment or exactly how they are interacting. But sequence-based ecological studies nearly always use a comparative approach, and that requires relevant reference sequences, which are an extremely limited resource when it comes to microbial eukaryotes

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease