24 research outputs found

    On the formation of a Hawking-radiation photosphere around microscopic black holes

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    We show that once a black hole surpasses some critical temperature TcritT_{crit}, the emitted Hawking radiation interacts with itself and forms a nearly thermal photosphere. Using QED, we show that the dominant interactions are bremsstrahlung and electron-photon pair production, and we estimate Tcritme/α5/2T_{crit} \sim m_{e}/\alpha^{5/2}, which when calculated more precisely is found to be TcritT_{crit} \approx 45 GeV. The formation of the photosphere is purely a particle physics effect, and not a general relativistic effect, since the the photosphere forms roughly α4\alpha^{-4} Schwarzschild radii away from the black hole. The temperature TT of the photosphere decreases with distance from the black hole, and the outer surface is determined by the constraint TmeT\sim m_{e} (for the QED case), since this is the point at which electrons and positrons annihilate, and the remaining photons free stream to infinity. Observational consequences are discussed, and it is found that, although the QED photosphere will not affect the Page-Hawking limits on primordial black holes, which is most important for 100MeV black holes, the inclusion of QCD interactions may significantly effect this limit, since for QCD we estimate TcritΛQCDT_{crit}\sim \Lambda_{QCD}. The photosphere greatly reduces possibility of observing individual black holes with temperatures greater than TcritT_{crit}, since the high energy particles emitted from the black hole are processed through the photosphere to a lower energy, where the gamma ray background is much higher. The temperature of the plasma in the photosphere can be extremely high, and this offers interesting possibilities for processes such as symmetry restoration.Comment: Latex, 16 pages, 3 postscript figures, submitted to PRD. Also available at http://fnas08.fnal.gov

    Lepton Flavour Violating Leptonic/Semileptonic Decays of Charged Leptons in the Minimal Supersymmetric Standard Model

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    We consider the leptonic and semileptonic (SL) lepton flavour violating (LFV) decays of the charged leptons in the minimal supersymmetric standard model (MSSM). The formalism for evaluation of branching fractions for the SL LFV charged-lepton decays with one or two pseudoscalar mesons, or one vector meson in the final state, is given. Previous amplitudes for the SL LFV charged-lepton decays in MSSM are improved, for instance the γ\gamma-penguin amplitude is corrected to assure the gauge invariance. The decays are studied not only in the model-independent formulation of the theory in the frame of MSSM, but also within the frame of the minimal supersymmetric SO(10) model within which the parameters of the MSSM are determined. The latter model gives predictions for the neutrino-Dirac Yukawa coupling matrix, once free parameters in the model are appropriately fixed to accommodate the recent neutrino oscillation data. Using this unambiguous neutrino-Dirac Yukawa couplings, we calculate the LFV leptonic and SL decay processes assuming the minimal supergravity scenario. A very detailed numerical analysis is done to constrain the MSSM parameters. Numerical results for SL LFV processes are given, for instance for tau -> e (mu) pi0, tau -> e (mu) eta, tau -> e (mu) eta', tau -> e (mu) rho0, tau -> e (mu) phi, tau -> e (mu) omega, etc.Comment: 36 pages, 3 tables, 5 .eps figure

    Formation of dense partonic matter in relativistic nucleus-nucleus collisions at RHIC: Experimental evaluation by the PHENIX collaboration

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    Extensive experimental data from high-energy nucleus-nucleus collisions were recorded using the PHENIX detector at the Relativistic Heavy Ion Collider (RHIC). The comprehensive set of measurements from the first three years of RHIC operation includes charged particle multiplicities, transverse energy, yield ratios and spectra of identified hadrons in a wide range of transverse momenta (p_T), elliptic flow, two-particle correlations, non-statistical fluctuations, and suppression of particle production at high p_T. The results are examined with an emphasis on implications for the formation of a new state of dense matter. We find that the state of matter created at RHIC cannot be described in terms of ordinary color neutral hadrons.Comment: 510 authors, 127 pages text, 56 figures, 1 tables, LaTeX. Submitted to Nuclear Physics A as a regular article; v3 has minor changes in response to referee comments. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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