How to Open a File and Not Get Hacked

Careless attention to opening files, often caused by prob-lems with path traversal or shared directories, can expose applications to attacks on the file names that they use. In this paper we present criteria to determine if a path is safe from attack and how previous algorithms are not sufficient to protect against such attacks. We then describe an algo-rithm to safely open a file when in the presence of an attack (and how to detect the presence of such an attack), and pro-vide a new library of file open routines that embodies our algorithm. These routines can be used as one-for-one sub-stitutes for conventional POSIX open and fopen calls. 1

New insights in dermatophyte research

Dermatophyte research has renewed interest because of changing human floras with changing socioeconomic conditions, and because of severe chronic infections in patients with congenital immune disorders. Main taxonomic traits at the generic level have changed considerably, and now fine-tuning at the species level with state-of-the-art technology has become urgent. Research on virulence factors focuses on secreted proteases now has support in genome data. It is speculated that most protease families are used for degrading hard keratin during nitrogen recycling in the environment, while others, such as Sub6 may have emerged as a result of ancestral gene duplication, and are likely to have specific roles during infection. Virulence may differ between mating partners of the same species and concepts of zoo- and anthropophily may require revision in some recently redefined species. Many of these questions benefit from international cooperation and exchange of materials. The aim of the ISHAM Working Group Dermatophytes aims to stimulate and coordinate international networking on these fungi

Initial correlations effects on decoherence at zero temperature

We consider a free charged particle interacting with an electromagnetic bath at zero temperature. The dipole approximation is used to treat the bath wavelengths larger than the width of the particle wave packet. The effect of these wavelengths is described then by a linear Hamiltonian whose form is analogous to phenomenological Hamiltonians previously adopted to describe the free particle-bath interaction. We study how the time dependence of decoherence evolution is related with initial particle-bath correlations. We show that decoherence is related to the time dependent dressing of the particle. Moreover because decoherence induced by the T=0 bath is very rapid, we make some considerations on the conditions under which interference may be experimentally observed.Comment: 16 pages, 1 figur

Phase Diffusion in Quantum Dissipative Systems

We study the dynamics of the quantum phase distribution associated with the reduced density matrix of a system for a number of situations of practical importance, as the system evolves under the influence of its environment, interacting via a quantum nondemoliton type of coupling, such that there is decoherence without dissipation, as well as when it interacts via a dissipative interaction, resulting in decoherence as well as dissipation. The system is taken to be either a two-level atom (or equivalently, a spin-1/2 system) or a harmonic oscillator, and the environment is modeled as a bath of harmonic oscillators, starting out in a squeezed thermal state. The impact of the different environmental parameters on the dynamics of the quantum phase distribution for the system starting out in various initial states, is explicitly brought out. An interesting feature that emerges from our work is that the relationship between squeezing and temperature effects depends on the type of system-bath interaction. In the case of quantum nondemolition type of interaction, squeezing and temperature work in tandem, producing a diffusive effect on the phase distribution. In contrast, in case of a dissipative interaction, the influence of temperature can be counteracted by squeezing, which manifests as a resistence to randomization of phase. We make use of the phase distributions to bring out a notion of complementarity in atomic systems. We also study the dispersion of the phase using the phase distributions conditioned on particular initial states of the system.Comment: Accepted for publication in Physical Review A; changes in section V; 20 pages, 12 figure

Euclidean Supergravity in Terms of Dirac Eigenvalues

It has been recently shown that the eigenvalues of the Dirac operator can be considered as dynamical variables of Euclidean gravity. The purpose of this paper is to explore the possiblity that the eigenvalues of the Dirac operator might play the same role in the case of supergravity. It is shown that for this purpose some primary constraints on covariant phase space as well as secondary constraints on the eigenspinors must be imposed. The validity of primary constraints under covariant transport is further analyzed. It is show that in the this case restrictions on the tanget bundle and on the spinor bundle of spacetime arise. The form of these restrictions is determined under some simplifying assumptions. It is also shown that manifolds with flat curvature of tangent bundle and spinor bundle and spinor bundle satisfy these restrictons and thus they support the Dirac eigenvalues as global observables.Comment: Misprints and formulae corrected; to appear in Phys. Rev.

The Gisin-Percival stochastic Schrödinger equation from standard quantum filtering theory

We show that the quantum state diffusion equation of Gisin and Percival, driven by complex Wiener noise, is equivalent up to a global stochastic phase to quantum trajectory models. With an appropriate feedback scheme, we set up an analogue continuous measurement model with exactly simulates the Gisin-Percival quantum state diffusion.Comment: Originally submitted to a Theoretical Physics journal but rejected with the re-submission instructions to drop my discussion and references to the papers of Gisin and Percival, which I consider unethical. To be now submitted to an appropriate Mathematical Physics journal instea

Bim and Bmf synergize to induce apoptosis in Neisseria gonorrhoeae infection

Abstract: Bcl-2 family proteins including the pro-apoptotic BH3-only proteins are central regulators of apoptotic cell death. Here we show by a focused siRNA miniscreen that the synergistic action of the BH3-only proteins Bim and Bmf is required for apoptosis induced by infection with Neisseria gonorrhoeae (Ngo). While Bim and Bmf were associated with the cytoskeleton of healthy cells, they both were released upon Ngo infection. Loss of Bim and Bmf from the cytoskeleton fraction required the activation of Jun-N-terminal kinase-1 (JNK-1), which in turn depended on Rac-1. Depletion and inhibition of Rac-1, JNK-1, Bim, or Bmf prevented the activation of Bak and Bax and the subsequent activation of caspases. Apoptosis could be reconstituted in Bim-depleted and Bmf-depleted cells by additional silencing of antiapoptotic Mcl-1 and Bcl-XL, respectively. Our data indicate a synergistic role for both cytoskeletal-associated BH3-only proteins, Bim, and Bmf, in an apoptotic pathway leading to the clearance of Ngo-infected cells. Author Summary: A variety of physiological death signals, as well as pathological insults, trigger apoptosis, a genetically programmed form of cell death. Pathogens often induce host cell apoptosis to establish a successful infection. Neisseria gonorrhoeae (Ngo), the etiological agent of the sexually transmitted disease gonorrhoea, is a highly adapted obligate human-specific pathogen and has been shown to induce apoptosis in infected cells. Here we unveil the molecular mechanisms leading to apoptosis of infected cells. We show that Ngo-mediated apoptosis requires a special subset of proapoptotic proteins from the group of BH3-only proteins. BH3-only proteins act as stress sensors to translate toxic environmental signals to the initiation of apoptosis. In a siRNA-based miniscreen, we found Bim and Bmf, BH3-only proteins associated with the cytoskeleton, necessary to induce host cell apoptosis upon infection. Bim and Bmf inactivated different inhibitors of apoptosis and thereby induced cell death in response to infection. Our data unveil a novel pathway of infection-induced apoptosis that enhances our understanding of the mechanism by which BH3-only proteins control apoptotic cell death