Quantum Circuits for the Unitary Permutation Problem

We consider the Unitary Permutation problem which consists, given $n$ unitary gates $U_1, \ldots, U_n$ and a permutation $\sigma$ of $\{1,\ldots, n\}$, in applying the unitary gates in the order specified by $\sigma$, i.e. in performing $U_{\sigma(n)}\ldots U_{\sigma(1)}$. This problem has been introduced and investigated by Colnaghi et al. where two models of computations are considered. This first is the (standard) model of query complexity: the complexity measure is the number of calls to any of the unitary gates $U_i$ in a quantum circuit which solves the problem. The second model provides quantum switches and treats unitary transformations as inputs of second order. In that case the complexity measure is the number of quantum switches. In their paper, Colnaghi et al. have shown that the problem can be solved within $n^2$ calls in the query model and $\frac{n(n-1)}2$ quantum switches in the new model. We refine these results by proving that $n\log_2(n) +\Theta(n)$ quantum switches are necessary and sufficient to solve this problem, whereas $n^2-2n+4$ calls are sufficient to solve this problem in the standard quantum circuit model. We prove, with an additional assumption on the family of gates used in the circuits, that $n^2-o(n^{7/4+\epsilon})$ queries are required, for any $\epsilon >0$. The upper and lower bounds for the standard quantum circuit model are established by pointing out connections with the permutation as substring problem introduced by Karp.Comment: 8 pages, 5 figure

The proteins DotY and DotZ modulate the dynamics and localization of the type IVB coupling complex of Legionella pneumophila

Legionella pneumophila is an opportunistic pathogen infecting alveolar macrophages and protozoa species. Legionella utilizes a Type IV Secretion System (T4SS) to translocate over 300 effector proteins into its host cell. In a recent study, we isolated and solved the cryo-EM structure of the Type IV Coupling Complex (T4CC), a large cytoplasmic determinant associated with the inner membrane that recruits effector proteins for delivery to the T4SS for translocation. The T4CC is composed of a DotLMNYZ hetero-pentameric core from which the flexible IcmSW module flexibly protrudes. The DotY and DotZ proteins were newly reported members of this complex and their role remained elusive. In this study, we observed the effect of deleting DotY and DotZ on T4CC stability and localization. Furthermore, we found these two proteins are co-dependent, whereby the deletion of DotY resulted in DotZ absence from the coupling complex, and vice versa. Additional cryo-EM data analysis revealed the dynamic movement of the IcmSW module is modified by the DotY/Z proteins. We therefore determined the likely function of DotY and DotZ and revealed their importance on T4CC function

Mechanism of effector capture and delivery by the type IV secretion system from Legionella pneumophila

Legionella pneumophila is a bacterial pathogen that utilises a Type IV secretion (T4S) system to inject effector proteins into human macrophages. Essential to the recruitment and delivery of effectors to the T4S machinery is the membrane-embedded T4 coupling complex (T4CC). Here, we purify an intact T4CC from the Legionella membrane. It contains the DotL ATPase, the DotM and DotN proteins, the chaperone module IcmSW, and two previously uncharacterised proteins, DotY and DotZ. The atomic resolution structure reveals a DotLMNYZ hetero-pentameric core from which the flexible IcmSW module protrudes. Six of these hetero-pentameric complexes may assemble into a 1.6-MDa hexameric nanomachine, forming an inner membrane channel for effectors to pass through. Analysis of multiple cryo EM maps, further modelling and mutagenesis provide working models for the mechanism for binding and delivery of two essential classes of Legionella effectors, depending on IcmSW or DotM, respectively

773-4 Long Term Efficacy and Safety of Endovascular Low Dose Irradiation In a Swine Model of Restenosis After Angloplasty

Restenosis after balloon angioplasty is characterized by neointima formation. We have previously shown that ionizing radiation reduce neointima formation two weeks after angioplasty in a swine model of restenosis. To determine the durability of this effect and the long term safety after endovascular irradiation twenty one miniswine coronary arteries underwent overstretch balloon injury with a 3.5mm angioplasty balloon in the LAD, LCX and RCA. High energy 1921ridium source was introduced immediately by random assignment to deliver 700 or 1400 cGy in 14 injured coronary arteries (LAD and CX). Six months later an angiogram was performed, the animals were killed and the coronary arteries were perfusion fixed. Serial sections were stained with H&E, WG, MT then evaluated by histopathologic and morphometric techniques. Intimal area (IA) and area of intimal thickness corrected for the extent of injury (INFL) was measured in the irradiated and control arteries and compared with pigs that underwent the same treatment but were followed for 2 weeks only.ResultsAll treated arteries were patent with normal angiographic appearance. Lumen diameters at baseline and follow-up were similar. There was no difference in fibrosis at the adventitia, media, perivascular space or adjacent segments of myocardium of the irradiated arteries compared with control.Control700 cGy1400 cGyIN/FL 2Weeks0.59±0.230.42±0.15**0.17±0.16****IN/FL 6 Months0.50±0.20.35±0.18*0.31±0.16**IA 6 Months (mm)1.25±0.250.85±0.47***0.62±0.45**P values: control versus treatment group:*P=0.009**P<0.001***P=0.05.****P<0.0001ConclusionsEndovascular low dose irradiation in this model is safe andthe inhibitory effect of localized radiation on neointimal thickening (restenos is like) response to angioplasty is maintained at six months