Noncommutative geometry inspired black holes in higher dimensions at the LHC

When embedding models of noncommutative geometry inspired black holes into the peridium of large extra dimensions, it is natural to relate the noncommutativity scale to the higher-dimensional Planck scale. If the Planck scale is of the order of a TeV, noncommutative geometry inspired black holes could become accessible to experiments. In this paper, we present a detailed phenomenological study of the production and decay of these black holes at the Large Hadron Collider (LHC). Noncommutative inspired black holes are relatively cold and can be well described by the microcanonical ensemble during their entire decay. One of the main consequences of the model is the existence of a black hole remnant. The mass of the black hole remnant increases with decreasing mass scale associated with noncommutative and decreasing number of dimensions. The experimental signatures could be quite different from previous studies of black holes and remnants at the LHC since the mass of the remnant could be well above the Planck scale. Although the black hole remnant can be very heavy, and perhaps even charged, it could result in very little activity in the central detectors of the LHC experiments, when compared to the usual anticipated black hole signatures. If this type of noncommutative inspired black hole can be produced and detected, it would result in an additional mass threshold above the Planck scale at which new physics occurs.Comment: 21 pages, 7 figure

Microcanonical treatment of black hole decay at the Large Hadron Collider

This study of corrections to the canonical picture of black hole decay in large extra dimensions examines the effects of back-reaction corrected and microcanonical emission at the LHC. We provide statistical interpretations of the different multiparticle number densities in terms of black hole decay to standard model particles. Provided new heavy particles of mass near the fundamental Planck scale are not discovered, differences between these corrections and thermal decay will be insignificant at the LHC.Comment: small additions and clarifications, format for J. Phys.

Virus protein of mosaic disease of tobacco

Publication authorized February 9, 1939.Digitized 2007 AES.Includes bibliographical references (page 12)

Spin decoherence by spacetime curvature

A decoherence mechanism caused by spacetime curvature is discussed. The spin state of a particle is shown to decohere if only the particle moves in a curved spacetime. In particular, when a particle is near the event horizon of a black hole, an extremely rapid spin decoherence occurs for an observer who is static in a Killing time, however slow the particle's motion is.Comment: 13 pages, 2 figure

Properties of Entanglement Monotones for Three-Qubit Pure States

Various parameterizations for the orbits under local unitary transformations of three-qubit pure states are analyzed. The interconvertibility, symmetry properties, parameter ranges, calculability and behavior under measurement are looked at. It is shown that the entanglement monotones of any multipartite pure state uniquely determine the orbit of that state under local unitary transformations. It follows that there must be an entanglement monotone for three-qubit pure states which depends on the Kempe invariant defined in [Phys. Rev. A 60, 910 (1999)]. A form for such an entanglement monotone is proposed. A theorem is proved that significantly reduces the number of entanglement monotones that must be looked at to find the maximal probability of transforming one multipartite state to another.Comment: 14 pages, REVTe

Very high-energy observations of the two high-frequency peaked BL Lac objects 1ES 1218+304 and H 1426+428

We present results of very-high-energy gamma-ray observations (E > 160 GeV) of two high-frequency-peaked BL Lac (HBL) objects, 1ES 1218+304 and H 1426+428, with the Solar Tower Atmospheric Cherenkov Effect Experiment (STACEE). Both sources are very-high-energy gamma-ray emitters above 100 GeV, detected using ground-based Cherenkov telescopes. STACEE observations of 1ES 1218+304 and H 1426+428 did not produce detections; we present 99% CL flux upper limits for both sources, assuming spectral indices measured mostly at higher energies

Inflammasomes are important mediators of prostatic inflammation associated with BPH

Background: There is mounting evidence to support the role of inflammation in benign prostate hyperplasia (BPH), and a recent study reported expression of inflammasome derived cytokine IL-18 in prostate biopsy of BPH patients. Here we examined the expression of inflammasome-derived cytokines and activation of nucleotide-binding oligomerization domain-like receptor with pyrin domain protein 1 (NLRP) 1 inflammasome in a rat model of prostatic inflammation relevant to BPH. Methods: Prostatic inflammation was experimentally induced in three-month-old male Sprague-Dawley rats by intraprostatic injection (50 μL) of either 5 % formalin or saline (sham) into the ventral lobes of prostate. 7 days later, prostate and bladder tissue was harvested for analysis of inflammasome by Western blot, immunohistochemistry and downstream cytokine production by Milliplex. Results: Expression of interleukins, CXC and CC chemokines were elevated 2-15 fold in formalin injected prostate relative to sham. Significant expression of NLRP1 inflammasome components and caspase-1 in prostate were associated with significant elevation of pro and cleaved forms of IL-1β (25.50 ± 1.16 vs 3.05 ± 0.65 pg/mg of protein) and IL-18 (1646.15 ± 182.61 vs 304.67 ± 103.95 pg/mg of protein). Relative to prostate tissue, the cytokine expression in bladder tissue was much lower and did not involve inflammasome activation. Conclusions: Significant upregulation of NLRP1, caspase-1 and downstream cytokines (IL-18 and IL-1β) suggests that a NLRP1 inflammasome is assembled and activated in prostate tissue of this rat model. Recapitulation of findings from human BPH specimens suggests that the inflammasome may perpetuate the inflammatory state associated with BPH. Further clarification of these pathways may offer innovative therapeutic targets for BPH-related inflammation