Supermatrix Models

We investigate several matrix models based on super Lie algebras, osp(1|32,R), u(1|16,16) and gl(1|32,R). They are natural generalizations of IIB matrix model and were first proposed by Smolin. In particular, we study the supersymmetry structures of these models and discuss possible reductions to IIB matrix model. We also point out that diffeomorphism invariance is hidden in gauge theories on noncommutative space which are derived from matrix models. This symmetry is independent of the global SO(9,1) invariance in IIB matrix model and we report our trial to extend the global Lorentz invariance to local symmetry by introducing u(1|16,16) or gl(1|32,R) super Lie algebras.Comment: 34 pages, 3 figure

Curved-space classical solutions of a massive supermatrix model

We investigate here a supermatrix model with a mass term and a cubic interaction. It is based on the super Lie algebra osp(1|32,R), which could play a role in the construction of the eleven-dimensional M-theory. This model contains a massive version of the IIB matrix model, where some fields have a tachyonic mass term. Therefore, the trivial vacuum of this theory is unstable. However, this model possesses several classical solutions where these fields build noncommutative curved spaces and these solutions are shown to be energetically more favorable than the trivial vacuum. In particular, we describe in details two cases, the SO(3) \times SO(3) \times SO(3) (three fuzzy 2-spheres) and the SO(9) (fuzzy 8-sphere) classical backgrounds.Comment: 16 pages, no figure, v2: shortened and clarified version, v3: some minor typos correcte

Monte Carlo Studies of the GWW Phase Transition in Large-N Gauge Theories

In the study of the small ten-dimensional Schwarzschild blackhole, the blackhole to string transition is an important problem. In hep-th/0605041, a possible identification is made between the Gross-Witten-Wadia (GWW) type third-order large-N phase transition in the boundary gauge theory and the string-black hole transition in the bulk. In this paper, we exhibit the existence of the GWW transition by Monte Carlo simulation in the zero mode bosonic action of the finite-temperature N=4 SYM theory on S^3. Exhibiting this transition in the truncated but highly non-trivial gauge theory implies that in the vicinity of the critical temperature T_c, the system goes critical, and the fluctuations give rise to universal formulas derived in hep-th/0605041 We also discuss the issue of SO(6) R-symmetry breaking.Comment: 15 pages, 7 figures, eq. (3.10) corrected (v3), reference added (v4

Type I interferon protects neurons from prions in in vivo models

Infectious prions comprising abnormal prion protein, which is produced by structural conversion of normal prion protein, are responsible for transmissible spongiform encephalopathies including Creutzfeldt-Jakob disease in humans. Prions are infectious agents that do not possess a genome and the pathogenic protein was not thought to evoke any immune response. Although we previously reported that interferon regulatory factor 3 (IRF3) was likely to be involved in the pathogenesis of prion diseases, suggesting the protective role of host innate immune responses mediated by IRF3 signalling, this remained to be clarified. Here, we investigated the reciprocal interactions of type I interferon evoked by IRF3 activation and prion infection and found that infecting prions cause the suppression of endogenous interferon expression. Conversely, treatment with recombinant interferons in an ex vivo model was able to inhibit prion infection. In addition, cells and mice deficient in type I interferon receptor (subunit interferon alpha/beta receptor 1), exhibited higher susceptibility to 22L-prion infection. Moreover, in in vivo and ex vivo prion-infected models, treatment with RO8191, a selective type I interferon receptor agonist, inhibited prion invasion and prolonged the survival period of infected mice. Taken together, these data indicated that the interferon signalling interferes with prion propagation and some interferon-stimulated genes might play protective roles in the brain. These findings may allow for the development of new strategies to combat fatal diseases

Hyperefficient PrP Sc amplification of mouse-adapted BSE and scrapie strain by protein misfolding cyclic amplification technique.

Abnormal forms of prion protein (PrP(Sc)) accumulate via structural conversion of normal PrP (PrP(C)) in the progression of transmissible spongiform encephalopathy. Under cell-free conditions, the process can be efficiently replicated using in vitro PrP(Sc) amplification methods, including protein misfolding cyclic amplification. These methods enable ultrasensitive detection of PrP(Sc); however, there remain difficulties in utilizing them in practice. For example, to date, several rounds of protein misfolding cyclic amplification have been necessary to reach maximal sensitivity, which not only take several weeks, but also result in an increased risk of contamination. In this study, we sought to further promote the rate of PrP(Sc) amplification in the protein misfolding cyclic amplification technique using mouse transmissible spongiform encephalopathy models infected with either mouse-adapted bovine spongiform encephalopathy or mouse-adapted scrapie, Chandler strain. Here, we demonstrate that appropriate regulation of sonication dramatically accelerates PrP(Sc) amplification in both strains. In fact, we reached maximum sensitivity, allowing the ultrasensitive detection of < 1 LD(50) of PrP(Sc) in the diluted brain homogenates, after only one or two reaction rounds, and in addition, we detected PrP(Sc) in the plasma of mouse-adapted bovine spongiform encephalopathy-infected mice. We believe that these results will advance the establishment of a fast, ultrasensitive diagnostic test for transmissible spongiform encephalopathies.The definitive version is available at www.blackwell-synergy.co

Postmortem Quantitative Analysis of Prion Seeding Activity in the Digestive System

Human prion diseases are neurodegenerative disorders caused by prion protein. Although infectivity was historically detected only in the central nervous system and lymphoreticular tissues of patients with sporadic Creutzfeldt-Jakob disease, recent reports suggest that the seeding activity of Creutzfeldt-Jakob disease prions accumulates in various non-neuronal organs including the liver, kidney, and skin. Therefore, we reanalyzed autopsy samples collected from patients with sporadic and genetic human prion diseases and found that seeding activity exists in almost all digestive organs. Unexpectedly, activity in the esophagus reached a level of prion seeding activity close to that in the central nervous system in some CJD patients, indicating that the safety of endoscopic examinations should be reconsidered

A practical solution to the sign problem in a matrix model for dynamical compactification

The matrix model formulation of superstring theory offers the possibility to understand the appearance of 4d space-time from 10d as a consequence of spontaneous breaking of the SO(10) symmetry. Monte Carlo studies of this issue is technically difficult due to the so-called sign problem. We present a practical solution to this problem generalizing the factorization method proposed originally by two of the authors (K.N.A. and J.N.). Explicit Monte Carlo calculations and large-N extrapolations are performed in a simpler matrix model with similar properties, and reproduce quantitative results obtained previously by the Gaussian expansion method. Our results also confirm that the spontaneous symmetry breaking indeed occurs due to the phase of the fermion determinant, which vanishes for collapsed configurations. We clarify various generic features of this approach, which would be useful in applying it to other statistical systems with the sign problem.Comment: 44 pages, 64 figures, v2: some minor typos correcte

Ultrasensitive human prion detection in cerebrospinal fluid by real-time quaking-induced conversion.

The development of technologies for the in vitro amplification of abnormal conformations of prion protein (PrP(Sc)) has generated the potential for sensitive detection of prions. Here we developed a new PrP(Sc) amplification assay, called real-time quaking-induced conversion (RT-QUIC), which allows the detection of ≥1 fg of PrP(Sc) in diluted Creutzfeldt-Jakob disease (CJD) brain homogenate. Moreover, we assessed the technique first in a series of Japanese subjects and then in a blind study of 30 cerebrospinal fluid specimens from Australia, which achieved greater than 80% sensitivity and 100% specificity. These findings indicate the promising enhanced diagnostic capacity of RT-QUIC in the antemortem evaluation of suspected CJD