Time of arrival through interacting environments: Tunneling processes

We discuss the propagation of wave packets through interacting environments. Such environments generally modify the dispersion relation or shape of the wave function. To study such effects in detail, we define the distribution function P_{X}(T), which describes the arrival time T of a packet at a detector located at point X. We calculate P_{X}(T) for wave packets traveling through a tunneling barrier and find that our results actually explain recent experiments. We compare our results with Nelson's stochastic interpretation of quantum mechanics and resolve a paradox previously apparent in Nelson's viewpoint about the tunneling time.Comment: Latex 19 pages, 11 eps figures, title modified, comments and references added, final versio

Quantum Tunneling in the Wigner Representation

Time dependence for barrier penetration is considered in the phase space. An asymptotic phase-space propagator for nonrelativistic scattering on a one - dimensional barrier is constructed. The propagator has a form universal for various initial state preparations and local potential barriers. It is manifestly causal and includes time-lag effects and quantum spreading. Specific features of quantum dynamics which disappear in the standard semi-classical approximation are revealed. The propagator may be applied to calculation of the final momentum and coordinate distributions, for particles transmitted through or reflected from the potential barrier, as well as for elucidating the tunneling time problem.Comment: 18 pages, LATEX, no figure

Dwell-time distributions in quantum mechanics

Some fundamental and formal aspects of the quantum dwell time are reviewed, examples for free motion and scattering off a potential barrier are provided, as well as extensions of the concept. We also examine the connection between the dwell time of a quantum particle in a region of space and flux-flux correlations at the boundaries, as well as operational approaches and approximations to measure the flux-flux correlation function and thus the second moment of the dwell time, which is shown to be characteristically quantum, and larger than the corresponding classical moment even for freely moving particles.Comment: To appear in "Time in Quantum Mechanics, Vol. 2", Springer 2009, ed. by J. G. Muga, A. Ruschhaupt and A. del Camp

Dynamics of quantum trajectories in chaotic systems

Quantum trajectories defined in the de Broglie--Bohm theory provide a causal way to interpret physical phenomena. In this Letter, we use this formalism to analyze the short time dynamics induced by unstable periodic orbits in a classically chaotic system, a situation in which scars are known to play a very important role. We find that the topologies of the quantum orbits are much more complicated than that of the scarring and associated periodic orbits, since the former have quantum interference built in. Thus scar wave functions are necessary to analyze the corresponding dynamics. Moreover, these topologies imply different return routes to the vicinity of the initial positions, and this reflects in the existence of different contributions in each peak of the survival probability function.Comment: 7 pages, 4 figures. Accepted for publication in Europhysics Letter

Time of arrival in the presence of interactions

We introduce a formalism for the calculation of the time of arrival t at a space point for particles traveling through interacting media. We develop a general formulation that employs quantum canonical transformations from the free to the interacting cases to construct t in the context of the Positive Operator Valued Measures. We then compute the probability distribution in the times of arrival at a point for particles that have undergone reflection, transmission or tunneling off finite potential barriers. For narrow Gaussian initial wave packets we obtain multimodal time distributions of the reflected packets and a combination of the Hartman effect with unexpected retardation in tunneling. We also employ explicitly our formalism to deal with arrivals in the interaction region for the step and linear potentials.Comment: 20 pages including 5 eps figure

How much time does a tunneling particle spend in the barrier region?

The question in the title may be answered by considering the outcome of a ``weak measurement'' in the sense of Aharonov et al. Various properties of the resulting time are discussed, including its close relation to the Larmor times. It is a universal description of a broad class of measurement interactions, and its physical implications are unambiguous.Comment: 5 pages; no figure

Human annexin A6 interacts with influenza a virus protein M2 and negatively modulates infection

Copyright © 2012, American Society for Microbiology. All Rights ReservedThe influenza A virus M2 ion channel protein has the longest cytoplasmic tail (CT) among the three viral envelope proteins and is well conserved between different viral strains. It is accessible to the host cellular machinery after fusion with the endosomal membrane and during the trafficking, assembly, and budding processes. We hypothesized that identification of host cellular interactants of M2 CT could help us to better understand the molecular mechanisms regulating the M2-dependent stages of the virus life cycle. Using yeast two-hybrid screening with M2 CT as bait, a novel interaction with the human annexin A6 (AnxA6) protein was identified, and their physical interaction was confirmed by coimmunoprecipitation assay and a colocalization study of virus-infected human cells. We found that small interfering RNA (siRNA)-mediated knockdown of AnxA6 expression significantly increased virus production, while its overexpression could reduce the titer of virus progeny, suggesting a negative regulatory role for AnxA6 during influenza A virus infection. Further characterization revealed that AnxA6 depletion or overexpression had no effect on the early stages of the virus life cycle or on viral RNA replication but impaired the release of progeny virus, as suggested by delayed or defective budding events observed at the plasma membrane of virus-infected cells by transmission electron microscopy. Collectively, this work identifies AnxA6 as a novel cellular regulator that targets and impairs the virus budding and release stages of the influenza A virus life cycle.This work was supported by the Research Fund for the Control of Infectious Disease (project 09080892) of the Hong Kong Government, the Area of Excellence Scheme of the University Grants Committee (grant AoE/M-12/-06 of the Hong Kong Special Administrative Region, China), the French Ministry of Health, the RESPARI Pasteur Network

Eligibility for and outcome of treatment of latent tuberculosis infection in a cohort of HIV-infected people in Spain

<p>Abstract</p> <p>Background</p> <p>Previous studies have demonstrated the efficacy of treatment for latent tuberculosis infection (TLTBI) in persons infected with the human immunodeficiency virus, but few studies have investigated the operational aspects of implementing TLTBI in the co-infected population.The study objectives were to describe eligibility for TLTBI as well as treatment prescription, initiation and completion in an HIV-infected Spanish cohort and to investigate factors associated with treatment completion.</p> <p>Methods</p> <p>Subjects were prospectively identified between 2000 and 2003 at ten HIV hospital-based clinics in Spain. Data were obtained from clinical records. Associations were measured using the odds ratio (OR) and its 95% confidence interval (95% CI).</p> <p>Results</p> <p>A total of 1242 subjects were recruited and 846 (68.1%) were evaluated for TLTBI. Of these, 181 (21.4%) were eligible for TLTBI either because they were tuberculin skin test (TST) positive (121) or because their TST was negative/unknown but they were known contacts of a TB case or had impaired immunity (60). Of the patients eligible for TLTBI, 122 (67.4%) initiated TLTBI: 99 (81.1%) were treated with isoniazid for 6, 9 or 12 months; and 23 (18.9%) with short-course regimens including rifampin plus isoniazid and/or pyrazinamide. In total, 70 patients (57.4%) completed treatment, 39 (32.0%) defaulted, 7 (5.7%) interrupted treatment due to adverse effects, 2 developed TB, 2 died, and 2 moved away. Treatment completion was associated with having acquired HIV infection through heterosexual sex as compared to intravenous drug use (OR:4.6; 95% CI:1.4-14.7) and with having taken rifampin and pyrazinamide for 2 months as compared to isoniazid for 9 months (OR:8.3; 95% CI:2.7-24.9).</p> <p>Conclusions</p> <p>A minority of HIV-infected patients eligible for TLTBI actually starts and completes a course of treatment. Obstacles to successful implementation of this intervention need to be addressed.</p

Epidermal Growth Factor Receptor (EGFR) mutation analysis, gene expression profiling and EGFR protein expression in primary prostate cancer

<p>Abstract</p> <p>Background</p> <p>Activating mutations of the epidermal growth factor receptor (<it>EGFR</it>) confer sensitivity to the tyrosine kinase inhibitors (TKi), gefitinib and erlotinib. We analysed EGFR expression, EGFR mutation status and gene expression profiles of prostate cancer (PC) to supply a rationale for EGFR targeted therapies in this disease.</p> <p>Methods</p> <p>Mutational analysis of EGFR TK domain (exons from 18 to 21) and immunohistochemistry for EGFR were performed on tumour tissues derived from radical prostatectomy from 100 PC patients. Gene expression profiling using oligo-microarrays was also carried out in 51 of the PC samples.</p> <p>Results</p> <p>EGFR protein overexpression (EGFR_high) was found in 36% of the tumour samples, and mutations were found in 13% of samples. Patients with EGFR_hightumours experienced a significantly increased risk of biochemical relapse (hazard ratio-HR 2.52, p=0.02) compared with patients with tumours expressing low levels of EGFR (EGFR_low). Microarray analysis did not reveal any differences in gene expression between EGFR_highand EGFR_lowtumours. Conversely, in EGFR_hightumours, we were able to identify a 79 gene signature distinguishing mutated from non-mutated tumours. Additionally, 29 genes were found to be differentially expressed between mutated/EGFR_high(n=3) and mutated/EGFR_lowtumours (n=5). Four of the down-regulated genes, U19/EAF2, ABCC4, KLK3 and ANXA3 and one of the up-regulated genes, FOXC1, are involved in PC progression.</p> <p>Conclusions</p> <p>Based on our findings, we hypothesize that accurate definition of the EGFR status could improve prognostic stratification and we suggest a possible role for EGFR-directed therapies in PC patients. Having been generated in a relatively small sample of patients, our results warrant confirmation in larger series.</p