142 research outputs found

    Will we observe black holes at LHC?

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    The generalized uncertainty principle, motivated by string theory and non-commutative quantum mechanics, suggests significant modifications to the Hawking temperature and evaporation process of black holes. For extra-dimensional gravity with Planck scale O(TeV), this leads to important changes in the formation and detection of black holes at the the Large Hadron Collider. The number of particles produced in Hawking evaporation decreases substantially. The evaporation ends when the black hole mass is Planck scale, leaving a remnant and a consequent missing energy of order TeV. Furthermore, the minimum energy for black hole formation in collisions is increased, and could even be increased to such an extent that no black holes are formed at LHC energies.Comment: 5 pages, 2 figures. Minor changes to match version to appear in Class. Quant. Gra

    Black Holes at Future Colliders and Beyond: a Topical Review

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    One of the most dramatic consequences of low-scale (~1 TeV) quantum gravity in models with large or warped extra dimension(s) is copious production of mini black holes at future colliders and in ultra-high-energy cosmic ray collisions. Hawking radiation of these black holes is expected to be constrained mainly to our three-dimensional world and results in rich phenomenology. In this topical review we discuss the current status of astrophysical observations of black holes and selected aspects of mini black hole phenomenology, such as production at colliders and in cosmic rays, black hole decay properties, Hawking radiation as a sensitive probe of the dimensionality of extra space, as well as an exciting possibility of finding new physics in the decays of black holes.Comment: 31 pages, 10 figures To appear in the Journal of Physics

    Interferon-induced Transmembrane Protein 1 restricts replication of virus that enter cells via the plasma membrane.

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    The acute antiviral response is mediated by a family of interferon-stimulated genes (ISGs), providing cell-intrinsic immunity. Mutations in genes encoding these proteins are often associated with increased susceptibility to viral infections. One family of ISGs with antiviral function is the interferon-inducible transmembrane proteins (IFITMs), of which IFITM3 has been studied extensively. In contrast, IFITM1 has not been studied in detail. Since IFITM1 can localize to the plasma membrane, we investigated its function with a range of enveloped viruses thought to infect cells by fusion with the plasma membrane. Overexpression of IFITM1 prevented infection by a number of Paramyxoviridae and Pneumoviridae, including respiratory syncytial virus (RSV), mumps virus, and human metapneumovirus (HMPV). IFITM1 also restricted infection with an enveloped DNA virus that can enter via the plasma membrane, herpes simplex virus 1 (HSV-1). To test the importance of plasma membrane localization for IFITM1 function, we identified blocks of amino acids in the conserved intracellular loop (CIL) domain that altered the subcellular localization of the protein and reduced antiviral activity. By screening reported data sets, 12 rare nonsynonymous single nucleotide polymorphisms (SNPs) were identified in human IFITM1, some of which are in the CIL domain. Using an Ifitm1-/- mouse, we show that RSV infection was more severe, thereby extending the range of viruses restricted in vivo by IFITM proteins and suggesting overall that IFITM1 is broadly antiviral and that this antiviral function is associated with cell surface localization.IMPORTANCE Host susceptibility to viral infection is multifactorial, but early control of viruses not previously encountered is predominantly mediated by the interferon-stimulated gene (ISG) family. There are upwards of 300 of these genes, the majority of which do not have a clearly defined function or mechanism of action. The cellular location of these proteins may have an important effect on their function. One ISG located at the plasma membrane is interferon-inducible transmembrane protein 1 (IFITM1). Here we demonstrate that IFITM1 can inhibit infection with a range of viruses that enter via the plasma membrane. Mutant IFITM1 proteins that were unable to localize to the plasma membrane did not restrict viral infection. We also observed for the first time that IFITM1 plays a role in vivo, and Ifitm1-/- mice were more susceptible to viral lung infection. These data contribute to our understanding of how ISGs prevent viral infections

    Teaching a Prisoner to Fish: Getting Tough on Crime by Preparing Prisoners to Reenter Society

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