The spinorial geometry of supersymmetric heterotic string backgrounds

We determine the geometry of supersymmetric heterotic string backgrounds for which all parallel spinors with respect to the connection $\hat\nabla$ with torsion $H$, the NS$\otimes$NS three-form field strength, are Killing. We find that there are two classes of such backgrounds, the null and the timelike. The Killing spinors of the null backgrounds have stability subgroups K\ltimes\bR^8 in $Spin(9,1)$, for $K=Spin(7)$, SU(4), $Sp(2)$, $SU(2)\times SU(2)$ and $\{1\}$, and the Killing spinors of the timelike backgrounds have stability subgroups $G_2$, SU(3), SU(2) and $\{1\}$. The former admit a single null $\hat\nabla$-parallel vector field while the latter admit a timelike and two, three, five and nine spacelike $\hat\nabla$-parallel vector fields, respectively. The spacetime of the null backgrounds is a Lorentzian two-parameter family of Riemannian manifolds $B$ with skew-symmetric torsion. If the rotation of the null vector field vanishes, the holonomy of the connection with torsion of $B$ is contained in $K$. The spacetime of time-like backgrounds is a principal bundle $P$ with fibre a Lorentzian Lie group and base space a suitable Riemannian manifold with skew-symmetric torsion. The principal bundle is equipped with a connection $\lambda$ which determines the non-horizontal part of the spacetime metric and of $H$. The curvature of $\lambda$ takes values in an appropriate Lie algebra constructed from that of $K$. In addition $dH$ has only horizontal components and contains the Pontrjagin class of $P$. We have computed in all cases the Killing spinor bilinears, expressed the fluxes in terms of the geometry and determine the field equations that are implied by the Killing spinor equations.Comment: 73pp. v2: minor change

Understanding Galaxy Formation and Evolution

The old dream of integrating into one the study of micro and macrocosmos is now a reality. Cosmology, astrophysics, and particle physics intersect in a scenario (but still not a theory) of cosmic structure formation and evolution called Lambda Cold Dark Matter (LCDM) model. This scenario emerged mainly to explain the origin of galaxies. In these lecture notes, I first present a review of the main galaxy properties, highlighting the questions that any theory of galaxy formation should explain. Then, the cosmological framework and the main aspects of primordial perturbation generation and evolution are pedagogically detached. Next, I focus on the ``dark side'' of galaxy formation, presenting a review on LCDM halo assembling and properties, and on the main candidates for non-baryonic dark matter. It is shown how the nature of elemental particles can influence on the features of galaxies and their systems. Finally, the complex processes of baryon dissipation inside the non-linearly evolving CDM halos, formation of disks and spheroids, and transformation of gas into stars are briefly described, remarking on the possibility of a few driving factors and parameters able to explain the main body of galaxy properties. A summary and a discussion of some of the issues and open problems of the LCDM paradigm are given in the final part of these notes.Comment: 50 pages, 10 low-resolution figures (for normal-resolution, DOWNLOAD THE PAPER (PDF, 1.9 Mb) FROM http://www.astroscu.unam.mx/~avila/avila.pdf). Lectures given at the IV Mexican School of Astrophysics, July 18-25, 2005 (submitted to the Editors on March 15, 2006

Detectability of Tensor Perturbations Through CBR Anisotropy (final published version)

Detection of the tensor perturbations predicted in inflationary models is important for testing inflation as well as for reconstructing the inflationary potential. We show that because of cosmic variance the tensor contribution to the square of the CBR quadrupole anisotropy must be greater than about 20\% of the scalar contribution to ensure a statistically significant detection of tensor perturbations. This sensitivity could be achieved by full-sky measurements on angular scales of $3^{\circ}$ and $0.5^\circ$.Comment: 10 pages, uu-encoded postscript file, FERMILAB-PUB-94/175-

Factors Associated with Revision Surgery after Internal Fixation of Hip Fractures

Background: Femoral neck fractures are associated with high rates of revision surgery after management with internal fixation. Using data from the Fixation using Alternative Implants for the Treatment of Hip fractures (FAITH) trial evaluating methods of internal fixation in patients with femoral neck fractures, we investigated associations between baseline and surgical factors and the need for revision surgery to promote healing, relieve pain, treat infection or improve function over 24 months postsurgery. Additionally, we investigated factors associated with (1) hardware removal and (2) implant exchange from cancellous screws (CS) or sliding hip screw (SHS) to total hip arthroplasty, hemiarthroplasty, or another internal fixation device. Methods: We identified 15 potential factors a priori that may be associated with revision surgery, 7 with hardware removal, and 14 with implant exchange. We used multivariable Cox proportional hazards analyses in our investigation. Results: Factors associated with increased risk of revision surgery included: female sex, [hazard ratio (HR) 1.79, 95% confidence interval (CI) 1.25-2.50; P = 0.001], higher body mass index (fo

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