Measurement of one-photon and two-photon wavepackets in spontaneous parametric down-conversion

One-photon and two-photon wavepackets of entangled two-photon states in spontaneous parametric down-conversion (SPDC) fields are calculated and measured experimentally. For type-II SPDC, measured one-photon and two-photon wavepackets agree well with theory. For type-I SPDC, the measured one-photon wavepacket agree with the theory. However, the two-photon wavepacket is much bigger than the expected value and the visibility of interference is low. We identify the sources of this discrepancy as the spatial filtering of the two-photon bandwidth and non-pair detection events caused by the detector apertures and the tuning curve characteristics of the type-I SPDC.Comment: 8 pages, two-column, to appear in J. Opt. Soc. Am.

Photon tunneling through absorbing dielectric barriers

Using a recently developed formalism of quantization of radiation in the presence of absorbing dielectric bodies, the problem of photon tunneling through absorbing barriers is studied. The multilayer barriers are described in terms of multistep complex permittivities in the frequency domain which satisfy the Kramers--Kronig relations. From the resulting input--output relations it is shown that losses in the layers may considerably change the photon tunneling times observed in two-photon interference experiments. It is further shown that for sufficiently large numbers of layers interference fringes are observed that cannot be related to a single traversal time.Comment: 17 pages LaTeX, 9 figures (PS) include

Nonlocal Dispersion Cancellation using Entangled Photons

A pair of optical pulses traveling through two dispersive media will become broadened and, as a result, the degree of coincidence between the optical pulses will be reduced. For a pair of entangled photons, however, nonlocal dispersion cancellation in which the dispersion experienced by one photon cancels the dispersion experienced by the other photon is possible. In this paper, we report an experimental demonstration of nonlocal dispersion cancellation using entangled photons. The degree of two-photon coincidence is shown to increase beyond the limit attainable without entanglement. Our results have important applications in fiber-based quantum communication and quantum metrology.Comment: 8 pages, 5 figure

On the equivalence of the Langevin and auxiliary field quantization methods for absorbing dielectrics

Recently two methods have been developed for the quantization of the electromagnetic field in general dispersing and absorbing linear dielectrics. The first is based upon the introduction of a quantum Langevin current in Maxwell's equations [T. Gruner and D.-G. Welsch, Phys. Rev. A 53, 1818 (1996); Ho Trung Dung, L. Kn\"{o}ll, and D.-G. Welsch, Phys. Rev. A 57, 3931 (1998); S. Scheel, L. Kn\"{o}ll, and D.-G. Welsch, Phys. Rev. A 58, 700 (1998)], whereas the second makes use of a set of auxiliary fields, followed by a canonical quantization procedure [A. Tip, Phys. Rev. A 57, 4818 (1998)]. We show that both approaches are equivalent.Comment: 7 pages, RevTeX, no figure

Dynamical properties of Au from tight-binding molecular-dynamics simulations

We studied the dynamical properties of Au using our previously developed tight-binding method. Phonon-dispersion and density-of-states curves at T=0 K were determined by computing the dynamical-matrix using a supercell approach. In addition, we performed molecular-dynamics simulations at various temperatures to obtain the temperature dependence of the lattice constant and of the atomic mean-square-displacement, as well as the phonon density-of-states and phonon-dispersion curves at finite temperature. We further tested the transferability of the model to different atomic environments by simulating liquid gold. Whenever possible we compared these results to experimental values.Comment: 7 pages, 9 encapsulated Postscript figures, submitted to Physical Review

Trans Fatty Acids Induce Vascular Inflammation and Reduce Vascular Nitric Oxide Production in Endothelial Cells

Intake of trans fatty acids (TFA), which are consumed by eating foods made from partially hydrogenated vegetable oils, is associated with a higher risk of cardiovascular disease. This relation can be explained by many factors including TFA's negative effect on endothelial function and reduced nitric oxide (NO) bioavailability. In this study we investigated the effects of three different TFA (2 common isomers of C18 found in partially hydrogenated vegetable oil and a C18 isomer found from ruminant-derived—dairy products and meat) on endothelial NF-κB activation and nitric oxide (NO) production. Human endothelial cells were treated with increasing concentrations of Elaidic (trans-C18:1 (9 trans)), Linoelaidic (trans-C18:2 (9 trans, 12 trans)), and Transvaccenic (trans-C18:1 (11 trans)) for 3 h. Both Elaidic and Linoelaidic acids were associated with increasing NF-κB activation as measured by IL-6 levels and phosphorylation of IκBα, and impairment of endothelial insulin signaling and NO production, whereas Transvaccenic acid was not associated with these responses. We also measured superoxide production, which has been hypothesized to be necessary in fatty acid-dependent activation of NF-κB. Both Elaidic acid and Linoelaidic acid are associated with increased superoxide production, whereas Transvaccenic acid (which did not induce inflammatory responses) did not increase superoxide production. We observed differential activation of endothelial superoxide production, NF-κB activation, and reduction in NO production by different C18 isomers suggesting that the location and number of trans double bonds effect endothelial NF-κB activation

Red wine polyphenols prevent metabolic and cardiovascular alterations associated with obesity in Zucker fatty rats (Fa/Fa)

Peer reviewedPublisher PD

Defective sphingosine-1-phosphate receptor 1 (S1P1) phosphorylation exacerbates TH17-mediated autoimmune neuroinflammation

Sphingosine-1-phosphate (S1P) signaling regulates lymphocyte egress from lymphoid organs into systemic circulation. Sphingosine phosphate receptor 1 (S1P1) agonist, FTY-720 (Gilenya™) arrests immune trafficking and prevents multiple sclerosis (MS) relapses. However, alternative mechanisms of S1P-S1P1 signaling have been reported. Phosphoproteomic analysis of MS brain lesions revealed S1P1 phosphorylation on S351, a residue crucial for receptor internalization. Mutant mice harboring a S1pr1 gene encoding phosphorylation-deficient receptors [S1P1(S5A)] developed severe experimental autoimmune encephalomyelitis (EAE) due to T helper (TH) 17-mediated autoimmunity in the peripheral immune and nervous system. S1P1 directly activated Janus-like kinase–signal transducer and activator of transcription 3 (JAK-STAT3) pathway via interleukin 6 (IL-6). Impaired S1P1 phosphorylation enhances TH17 polarization and exacerbates autoimmune neuroinflammation. These mechanisms may be pathogenic in MS

Lymphocytes Accelerate Epithelial Tight Junction Assembly: Role of AMP-Activated Protein Kinase (AMPK)

The tight junctions (TJs), characteristically located at the apicolateral borders of adjacent epithelial cells, are required for the proper formation of epithelial cell polarity as well as for sustaining the mucosal barrier to the external environment. The observation that lymphocytes are recruited by epithelial cells to the sites of infection [1] suggests that they may play a role in the modulation of epithelial barrier function and thus contribute to host defense. To test the ability of lymphocytes to modulate tight junction assembly in epithelial cells, we set up a lymphocyte-epithelial cell co-culture system, in which Madin-Darby canine kidney (MDCK) cells, a well-established model cell line for studying epithelial TJ assembly [2], were co-cultured with mouse lymphocytes to mimic an infection state. In a typical calcium switch experiment, the TJ assembly in co-culture was found to be accelerated compared to that in MDCK cells alone. This accelaration was found to be mediated by AMP-activated protein kinase (AMPK). AMPK activation was independent of changes in cellular ATP levels but it was found to be activated by the pro-inflammatory cytokine TNF-α. Forced suppression of AMPK, either with a chemical inhibitor or by knockdown, abrogated the accelerating effect of lymphocytes on TJ formation. Similar results were also observed in a co-culture with lymphocytes and Calu-3 human airway epithelial cells, suggesting that the activation of AMPK may be a general mechanism underlying lymphocyte-accelerated TJ assembly in different epithelia. These results suggest that signals from lymphocytes, such as cytokines, facilitate TJ assembly in epithelial cells via the activation of AMPK