A quantum central limit theorem for non-equilibrium systems: Exact local relaxation of correlated states

We prove that quantum many-body systems on a one-dimensional lattice locally relax to Gaussian states under non-equilibrium dynamics generated by a bosonic quadratic Hamiltonian. This is true for a large class of initial states - pure or mixed - which have to satisfy merely weak conditions concerning the decay of correlations. The considered setting is a proven instance of a situation where dynamically evolving closed quantum systems locally appear as if they had truly relaxed, to maximum entropy states for fixed second moments. This furthers the understanding of relaxation in suddenly quenched quantum many-body systems. The proof features a non-commutative central limit theorem for non-i.i.d. random variables, showing convergence to Gaussian characteristic functions, giving rise to trace-norm closeness. We briefly relate our findings to ideas of typicality and concentration of measure.Comment: 27 pages, final versio

La Paloma : La Colombe

https://digitalcommons.library.umaine.edu/mmb-ps/3122/thumbnail.jp

Measuring entanglement in condensed matter systems

We show how entanglement may be quantified in spin and cold atom many-body systems using standard experimental techniques only. The scheme requires no assumptions on the state in the laboratory and a lower bound to the entanglement can be read off directly from the scattering cross section of Neutrons deflected from solid state samples or the time-of-flight distribution of cold atoms in optical lattices, respectively. This removes a major obstacle which so far has prevented the direct and quantitative experimental study of genuine quantum correlations in many-body systems: The need for a full characterization of the state to quantify the entanglement contained in it. Instead, the scheme presented here relies solely on global measurements that are routinely performed and is versatile enough to accommodate systems and measurements different from the ones we exemplify in this work.Comment: 6 pages, 2 figure

Handbook for estimating toxic fuel hazards

Computer program predicts, from readily available meteorological data, concentration and dosage fields downwind from ground-level and elevated sources of toxic fuel emissions. Mathematical model is applicable to hot plume rise from industrial stacks and should also be of interest to air pollution meteorologists

Anisotropic valence-->core x-ray fluorescence from a [Rh(en)3][Mn(N)(CN)5]·H2O single crystal: Experimental results and density functional calculations

High resolution x-ray fluorescence spectra have been recorded for emission in different directions from a single crystal of the compound [Rh(en)3][Mn(N)(CN)5]·H2O. The spectra are interpreted by comparison with density functional theory (DFT) electronic structure calculations. The Kbeta[double-prime] line, which is strongly polarized along the Mn–N axis, can be viewed as an N(2s)-->Mn(1s) transition, and the angular dependence is understood within the dipole approximation. The so-called Kbeta2,5 region has numerous contributions but is dominated by Mn(4p) and C(2s)-->Mn(1s) transitions. Transition energy splittings are found in agreement with those of calculated occupied molecular orbitals to within 1 eV. Computed relative transition probabilities reproduce experimentally observed trends

Structural basis of TFIIH activation for nucleotide excision repair.

Nucleotide excision repair (NER) is the major DNA repair pathway that removes UV-induced and bulky DNA lesions. There is currently no structure of NER intermediates, which form around the large multisubunit transcription factor IIH (TFIIH). Here we report the cryo-EM structure of an NER intermediate containing TFIIH and the NER factor XPA. Compared to its transcription conformation, the TFIIH structure is rearranged such that its ATPase subunits XPB and XPD bind double- and single-stranded DNA, consistent with their translocase and helicase activities, respectively. XPA releases the inhibitory kinase module of TFIIH, displaces a 'plug' element from the DNA-binding pore in XPD, and together with the NER factor XPG stimulates XPD activity. Our results explain how TFIIH is switched from a transcription to a repair factor, and provide the basis for a mechanistic analysis of the NER pathway