Crossing of the w=-1 barrier in viscous modified gravity

We consider a modified form of gravity in which the action contains a power alpha of the scalar curvature. It is shown how the presence of a bulk viscosity in a spatially flat universe may drive the cosmic fluid into the phantom region (w<-1) and thus into a Big Rip singularity, even if it lies in the quintessence region (w>-1) in the non-viscous case. The condition for this to occur is that the bulk viscosity contains the power (2 alpha-1) of the scalar expansion. Two specific examples are discussed in detail. The present paper is a generalization of the recent investigation dealing with barrier crossing in Einstein's gravity: I. Brevik and O. Gorbunova, Gen. Relativ. Grav. 37 (2005) 2039.Comment: 12 pages, latex, no figure

Inaccessible Singularities in Toral Cosmology

The familiar Bang/Crunch singularities of classical cosmology have recently been augmented by new varieties: rips, sudden singularities, and so on. These tend to be associated with final states. Here we consider an alternative possibility for the initial state: a singularity which has the novel property of being inaccessible to physically well-defined probes. These singularities arise naturally in cosmologies with toral spatial sections.Comment: 10 pages, version to appear in Classical and Quantum Gravit

How to find the holonomy algebra of a Lorentzian manifold

Manifolds with exceptional holonomy play an important role in string theory, supergravity and M-theory. It is explained how one can find the holonomy algebra of an arbitrary Riemannian or Lorentzian manifold. Using the de~Rham and Wu decompositions, this problem is reduced to the case of locally indecomposable manifolds. In the case of locally indecomposable Riemannian manifolds, it is known that the holonomy algebra can be found from the analysis of special geometric structures on the manifold. If the holonomy algebra $\mathfrak{g}\subset\mathfrak{so}(1,n-1)$ of a locally indecomposable Lorentzian manifold $(M,g)$ of dimension $n$ is different from $\mathfrak{so}(1,n-1)$, then it is contained in the similitude algebra $\mathfrak{sim}(n-2)$. There are 4 types of such holonomy algebras. Criterion how to find the type of $\mathfrak{g}$ are given, and special geometric structures corresponding to each type are described. To each $\mathfrak{g}$ there is a canonically associated subalgebra $\mathfrak{h}\subset\mathfrak{so}(n-2)$. An algorithm how to find $\mathfrak{h}$ is provided.Comment: 15 pages; the final versio

Why did IL-23p19 inhibition fail in AS: a tale of tissues, trials or translation?

No abstract available

Europe rules on harm from fluoroquinolone antibiotics

No abstract available

Introduction to Modified Gravity and Gravitational Alternative for Dark Energy

We review various modified gravities considered as gravitational alternative for dark energy. Specifically, we consider the versions of $f(R)$, $f(G)$ or $f(R,G)$ gravity, model with non-linear gravitational coupling or string-inspired model with Gauss-Bonnet-dilaton coupling in the late universe where they lead to cosmic speed-up. It is shown that some of such theories may pass the Solar System tests. On the same time, it is demonstrated that they have quite rich cosmological structure: they may naturally describe the effective (cosmological constant, quintessence or phantom) late-time era with a possible transition from decceleration to acceleration thanks to gravitational terms which increase with scalar curvature decrease. The possibility to explain the coincidence problem as the manifestation of the universe expansion in such models is mentioned. The late (phantom or quintessence) universe filled with dark fluid with inhomogeneous equation of state (where inhomogeneous terms are originated from the modified gravity) is also described.Comment: LaTeX file, 21 pages, references are added, lectures for 42 Karpacz Winter School on Theor Physic

Wounds that heal and wounds that don't - The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

IL-33 is a member of the IL-1 family of cytokines. IL-33 is predominantly located within the nucleus of cells where it plays a role in gene regulation. Given the right combination of signals and cellular damage, stored IL-33 is released from the cell where it can interact with its receptor ST2, triggering danger-associated responses and act as a cellular "alarmin". Whilst IL-33/ST2 signalling has been shown to induce potent pro-inflammatory responses that can be detrimental in certain disease states, a dichotomous, protective role of IL-33 in promoting wound healing has also emerged in multiple tissues types. This review will explore the current literature concerning this homeostatic role of IL-33/ST2 in tissue repair and also review its role in uncontrolled wound responses as seen in both fibrosis and tumorigenesis

The Strong Energy Condition and the S-Brane Singularity Problem

Recently it has been argued that, because tachyonic matter satisfies the Strong Energy Condition [SEC], there is little hope of avoiding the singularities which plague S-Brane spacetimes. Meanwhile, however, Townsend and Wohlfarth have suggested an ingenious way of circumventing the SEC in such situations, and other suggestions for actually violating it in the S-Brane context have recently been proposed. Of course, the natural context for discussions of [effective or actual] violations of the SEC is the theory of asymptotically deSitter spacetimes, which tend to be less singular than ordinary FRW spacetimes. However, while violating or circumventing the SEC is necessary if singularities are to be avoided, it is not at all clear that it is sufficient. That is, we can ask: would an asymptotically deSitter S-brane spacetime be non-singular? We show that this is difficult to achieve; this result is in the spirit of the recently proved "S-brane singularity theorem". Essentially our results suggest that circumventing or violating the SEC may not suffice to solve the S-Brane singularity problem, though we do propose two ways of avoiding this conclusion.Comment: 13 pages, minor corrections and improvements, references adde

MicroRNA29a regulates IL-33-mediated tissue remodelling in tendon disease

MicroRNA (miRNA) has the potential for cross-regulation and functional integration of discrete biological processes during complex physiological events. Utilizing the common human condition tendinopathy as a model system to explore the cross-regulation of immediate inflammation and matrix synthesis by miRNA we observed that elevated IL-33 expression is a characteristic of early tendinopathy. Using in vitro tenocyte cultures and in vivo models of tendon damage, we demonstrate that such IL-33 expression plays a pivotal role in the transition from type 1 to type 3 collagen (Col3) synthesis and thus early tendon remodelling. Both IL-33 effector function, via its decoy receptor sST2, and Col3 synthesis are regulated by miRNA29a. Downregulation of miRNA29a in human tenocytes is sufficient to induce an increase in Col3 expression. These data provide a molecular mechanism of miRNA-mediated integration of the early pathophysiologic events that facilitate tissue remodelling in human tendon after injury