3,602 research outputs found

    Polarization entangled photon-pair source based on quantum nonlinear photonics and interferometry

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    We present a versatile, high-brightness, guided-wave source of polarization entangled photons, emitted at a telecom wavelength. Photon-pairs are generated using an integrated type-0 nonlinear waveguide, and subsequently prepared in a polarization entangled state via a stabilized fiber interferometer. We show that the single photon emission wavelength can be tuned over more than 50 nm, whereas the single photon spectral bandwidth can be chosen at will over more than five orders of magnitude (from 25 MHz to 4 THz). Moreover, by performing entanglement analysis, we demonstrate a high degree of control of the quantum state via the violation of the Bell inequalities by more than 40 standard deviations. This makes this scheme suitable for a wide range of quantum optics experiments, ranging from fundamental research to quantum information applications. We report on details of the setup, as well as on the characterization of all included components, previously outlined in F. Kaiser et al. (2013 Laser Phys. Lett. 10, 045202).Comment: 16 pages, 7 figure

    apeNEXT: A multi-TFlops Computer for Simulations in Lattice Gauge Theory

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    We present the APE (Array Processor Experiment) project for the development of dedicated parallel computers for numerical simulations in lattice gauge theories. While APEmille is a production machine in today's physics simulations at various sites in Europe, a new machine, apeNEXT, is currently being developed to provide multi-Tflops computing performance. Like previous APE machines, the new supercomputer is largely custom designed and specifically optimized for simulations of Lattice QCD.Comment: Poster at the XXIII Physics in Collisions Conference (PIC03), Zeuthen, Germany, June 2003, 3 pages, Latex. PSN FRAP15. Replaced for adding forgotten autho

    Performance of a Tungsten-Cerium Fluoride Sampling Calorimeter in High-Energy Electron Beam Tests

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    A prototype for a sampling calorimeter made out of cerium fluoride crystals interleaved with tungsten plates, and read out by wavelength-shifting fibres, has been exposed to beams of electrons with energies between 20 and 150 GeV, produced by the CERN Super Proton Synchrotron accelerator complex. The performance of the prototype is presented and compared to that of a Geant4 simulation of the apparatus. Particular emphasis is given to the response uniformity across the channel front face, and to the prototype's energy resolution.Comment: 6 pages, 6 figures, Submitted to NIM

    Oral tolerance to cancer can be abrogated by T regulatory cell inhibition

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    Oral administration of tumour cells induces an immune hypo-responsiveness known as oral tolerance. We have previously shown that oral tolerance to a cancer is tumour antigen specific, non-cross-reactive and confers a tumour growth advantage. We investigated the utilisation of regulatory T cell (Treg) depletion on oral tolerance to a cancer and its ability to control tumour growth. Balb/C mice were gavage fed homogenised tumour tissue – JBS fibrosarcoma (to induce oral tolerance to a cancer), or PBS as control. Growth of subcutaneous JBS tumours were measured; splenic tissue excised and flow cytometry used to quantify and compare systemic Tregs and T effector (Teff) cell populations. Prior to and/or following tumour feeding, mice were intraperitoneally administered anti-CD25, to inactivate systemic Tregs, or given isotype antibody as a control. Mice which were orally tolerised prior to subcutaneous tumour induction, displayed significantly higher systemic Treg levels (14% vs 6%) and faster tumour growth rates than controls (p<0.05). Complete regression of tumours were only seen after Treg inactivation and occurred in all groups - this was not inhibited by tumour feeding. The cure rates for Treg inactivation were 60% during tolerisation, 75% during tumour growth and 100% during inactivation for both tolerisation and tumour growth. Depletion of Tregs gave rise to an increased number of Teff cells. Treg depletion post-tolerisation and post-tumour induction led to the complete regression of all tumours on tumour bearing mice. Oral administration of tumour tissue, confers a tumour growth advantage and is accompanied by an increase in systemic Treg levels. The administration of anti-CD25 Ab decreased Treg numbers and caused an increase in Teffs. Most notably Treg cell inhibition overcame established oral tolerance with consequent tumor regression, especially relevant to foregut cancers where oral tolerance is likely to be induced by the shedding of tumour tissue into the gut

    Predicting 2-drug antiretroviral regimen efficacy by genotypic susceptibility score: results from a cohort study

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    Background: HIV drug resistance has a deleterious effect on the virological outcome of antiretroviral therapy (ART). The aim of the study was to evaluate the ability of genotypic susceptibility score (GSS) to predict virological outcome following an ART switch to a 2-drug regimen in virosuppressed HIV-1 infected patients. Material and methods: From the ARCA database we selected HIV-1 infected patients virologically suppressed switching to 2-drug ART (2006-2018, time of switch=baseline), with pre-baseline resistance genotype and at least one HIV-1 RNA determination during follow up. Primary endopoint was virological failure (VF: an HIV-RNA, VL, ≥ 200 cps/mL or 2 consecutive ≥ 50 cps/mL). Survival analysis was used to investigate predictors of VF. The GSS predicted by the latest and the cumulative genotype (CGSS) was calculated using the Stanford hivdb (v.8.5) with respect to the 2-drug regimen started. CD4 changes from baseline at weeks 24, 48 and 96 were assessed using Student’s t-test for paired samples. Results: We included 773 patients: 522 (68%) were males, 186 (24%) heterosexuals, with median age of 50 years (IQR, 43-56), 10 years of HIV (5-20), 7 years of ART (4-15) and 5 (3-8) previous antiretroviral (ARV) lines. At baseline patients had been virologically suppressed for 6.4 years (2.5-14), allowing isolated blips. The median zenith VL was 4.9 log10 (4.4-5.5), CD4 cells count at nadir 222 (108-324) and at baseline 640 (477-860). Median GSS was 2 (1.5-2), with GSS &lt;2 in 213 (28%) pts, median CGSS was 2 (1-2), with CGSS &lt;2 in 250 (33%). The previous ARV classes used were NRTI in 770 patients (99%), NNRTI in 416 (54%), boosted PI in 639 (83%) and INSTI in 218 (28%). Current ARV regimens included: PI+3TC in 455 pts (59%), of which 3TC+ ATV unboosted or ATV/r or ATV/c in 181 (23%) and DRV/r or DRV/c in 274 (36%), DTG+3TC in 260 (34%) and DTG+RPV in 58 (7%). During a median observation time of 75 wks (IQR 37-120) the estimated probability of VF at 48 weeks was 6% (95% CI 5-7) among patients with GSS=2, 4% (3-5) among patients with GSS 1-1.99 and 11% (4-18) among those with GSS &lt;1 (Log Rank p=0.21). According to CGSS, the estimated probability of VF at 48 weeks was 5% (95% CI 1-6) among patients with CGSS =2, 6% (4-8) among patients with CGSS 1-1.99 and 8% (3-13) among those with CGSS &lt;1 (Log Rank p=0.006) (Fig 1). Observed median changes of CD4+ counts from baseline were +24 cells/μL (IQR -67;+132) at 24 weeks, +49 cells/μL (IQR -31;+159) at 48 weeks and +74 cells/μL (IQR -30; +197) at 96 weeks (p&lt;0.001 for all comparisons). At multivariate analysis, adjusting for years of ART, CD4 cell count at nadir and at baseline, CGSS strata, number of previous ARV lines, only longer time since last VL&gt;50 cps/mL was associated with lower risk of VF (+ 1 year, aHR 0.89, 95% CI 0.82-0.98; p=0.01). Conclusions: Despite an effect of CGSS, the duration of virosuppression was the only independent predictor of virological efficacy of switching to 2-drug regimens
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