Formulas and equations for finding scattering data from the Dirichlet-to-Neumann map with nonzero background potential

For the Schrodinger equation at fixed energy with a potential supported in a bounded domain we give formulas and equations for finding scattering data from the Dirichlet-to-Neumann map with nonzero background potential. For the case of zero background potential these results were obtained in [R.G.Novikov, Multidimensional inverse spectral problem for the equation -\Delta\psi+(v(x)-Eu(x))\psi=0, Funkt. Anal. i Ego Prilozhen 22(4), pp.11-22, (1988)]

New global stability estimates for the Gel'fand-Calderon inverse problem

We prove new global stability estimates for the Gel'fand-Calderon inverse problem in 3D. For sufficiently regular potentials this result of the present work is a principal improvement of the result of [G. Alessandrini, Stable determination of conductivity by boundary measurements, Appl. Anal. 27 (1988), 153-172]

A convergent algorithm for the hybrid problem of reconstructing conductivity from minimal interior data

We consider the hybrid problem of reconstructing the isotropic electric conductivity of a body $\Omega$ from interior Current Density Imaging data obtainable using MRI measurements. We only require knowledge of the magnitude $|J|$ of one current generated by a given voltage $f$ on the boundary $\partial\Omega$. As previously shown, the corresponding voltage potential u in $\Omega$ is a minimizer of the weighted least gradient problem $$u=\hbox{argmin} \{\int_{\Omega}a(x)|\nabla u|: u \in H^{1}(\Omega), \ \ u|_{\partial \Omega}=f\},$$ with $a(x)= |J(x)|$. In this paper we present an alternating split Bregman algorithm for treating such least gradient problems, for $a\in L^2(\Omega)$ non-negative and $f\in H^{1/2}(\partial \Omega)$. We give a detailed convergence proof by focusing to a large extent on the dual problem. This leads naturally to the alternating split Bregman algorithm. The dual problem also turns out to yield a novel method to recover the full vector field $J$ from knowledge of its magnitude, and of the voltage $f$ on the boundary. We then present several numerical experiments that illustrate the convergence behavior of the proposed algorithm

Inverse problems with partial data for a magnetic Schr\"odinger operator in an infinite slab and on a bounded domain

In this paper we study inverse boundary value problems with partial data for the magnetic Schr\"odinger operator. In the case of an infinite slab in $R^n$, $n\ge 3$, we establish that the magnetic field and the electric potential can be determined uniquely, when the Dirichlet and Neumann data are given either on the different boundary hyperplanes of the slab or on the same hyperplane. This is a generalization of the results of [41], obtained for the Schr\"odinger operator without magnetic potentials. In the case of a bounded domain in $R^n$, $n\ge 3$, extending the results of [2], we show the unique determination of the magnetic field and electric potential from the Dirichlet and Neumann data, given on two arbitrary open subsets of the boundary, provided that the magnetic and electric potentials are known in a neighborhood of the boundary. Generalizing the results of [31], we also obtain uniqueness results for the magnetic Schr\"odinger operator, when the Dirichlet and Neumann data are known on the same part of the boundary, assuming that the inaccessible part of the boundary is a part of a hyperplane

Evidence for Pervasive Adaptive Protein Evolution in Wild Mice

The relative contributions of neutral and adaptive substitutions to molecular evolution has been one of the most controversial issues in evolutionary biology for more than 40 years. The analysis of within-species nucleotide polymorphism and between-species divergence data supports a widespread role for adaptive protein evolution in certain taxa. For example, estimates of the proportion of adaptive amino acid substitutions (alpha) are 50% or more in enteric bacteria and Drosophila. In contrast, recent estimates of alpha for hominids have been at most 13%. Here, we estimate alpha for protein sequences of murid rodents based on nucleotide polymorphism data from multiple genes in a population of the house mouse subspecies Mus musculus castaneus, which inhabits the ancestral range of the Mus species complex and nucleotide divergence between M. m. castaneus and M. famulus or the rat. We estimate that 57% of amino acid substitutions in murids have been driven by positive selection. Hominids, therefore, are exceptional in having low apparent levels of adaptive protein evolution. The high frequency of adaptive amino acid substitutions in wild mice is consistent with their large effective population size, leading to effective natural selection at the molecular level. Effective natural selection also manifests itself as a paucity of effectively neutral nonsynonymous mutations in M. m. castaneus compared to humans

The role of mutation rate variation and genetic diversity in the architecture of human disease

Background We have investigated the role that the mutation rate and the structure of genetic variation at a locus play in determining whether a gene is involved in disease. We predict that the mutation rate and its genetic diversity should be higher in genes associated with disease, unless all genes that could cause disease have already been identified. Results Consistent with our predictions we find that genes associated with Mendelian and complex disease are substantially longer than non-disease genes. However, we find that both Mendelian and complex disease genes are found in regions of the genome with relatively low mutation rates, as inferred from intron divergence between humans and chimpanzees, and they are predicted to have similar rates of non-synonymous mutation as other genes. Finally, we find that disease genes are in regions of significantly elevated genetic diversity, even when variation in the rate of mutation is controlled for. The effect is small nevertheless. Conclusions Our results suggest that gene length contributes to whether a gene is associated with disease. However, the mutation rate and the genetic architecture of the locus appear to play only a minor role in determining whether a gene is associated with disease