Spacelike Branes

Scalar field theories with appropriate potentials in Minkowski space can have time-dependent classical solutions containing topological defects which correspond to S-branes - i.e. branes all of whose tangential dimensions are spacelike. It is argued that such S-branes arise in string theory as time-dependent solutions of the worldvolume tachyon field of an unstable D-brane or D-brane-anti-D-brane pair. Using the known coupling of the spacetime RR fields to the worldvolume tachyon it is shown that these S-branes carry a charge, defined as the integral of a RR field strength over a sphere (containing a time as well as spatial dimensions) surrounding the S-brane. This same charge is carried by SD-branes, i.e. Dirichlet branes arising from open string worldsheet conformal field theories with a Dirichlet boundary condition on the timelike dimension. The corresponding SD-brane boundary state is constructed. Supergravity solutions carrying the same charges are also found for a few cases.Comment: 23 pages, harvmac(b), no figures, v2 references added and minor changes, v4: more references adde

M-theory, Cosmological Constant and Anthropic Principle

We discuss the theory of dark energy based on maximally extended supergravity and suggest a possible anthropic explanation of the present value of the cosmological constant and of the observed ratio between dark energy and energy of matter.Comment: 8 pages, 6 figures, Introduction and Discussion are expande

Quantum walks: a comprehensive review

Quantum walks, the quantum mechanical counterpart of classical random walks, is an advanced tool for building quantum algorithms that has been recently shown to constitute a universal model of quantum computation. Quantum walks is now a solid field of research of quantum computation full of exciting open problems for physicists, computer scientists, mathematicians and engineers. In this paper we review theoretical advances on the foundations of both discrete- and continuous-time quantum walks, together with the role that randomness plays in quantum walks, the connections between the mathematical models of coined discrete quantum walks and continuous quantum walks, the quantumness of quantum walks, a summary of papers published on discrete quantum walks and entanglement as well as a succinct review of experimental proposals and realizations of discrete-time quantum walks. Furthermore, we have reviewed several algorithms based on both discrete- and continuous-time quantum walks as well as a most important result: the computational universality of both continuous- and discrete- time quantum walks.Comment: Paper accepted for publication in Quantum Information Processing Journa

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

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