Grassmann Variables and the Jaynes-Cummings Model

This paper shows that phase space methods using a positive P type distribution function involving both c-number variables (for the cavity mode) and Grassmann variables (for the two level atom) can be used to treat the Jaynes-Cummings model. Although it is a Grassmann function, the distribution function is equivalent to six c-number functions of the two bosonic variables. Experimental quantities are given as bosonic phase space integrals involving the six functions. A Fokker-Planck equation involving both left and right Grassmann differentiation can be obtained for the distribution function, and is equivalent to six coupled equations for the six c-number functions. The approach used involves choosing the canonical form of the (non-unique) positive P distribution function, where the correspondence rules for bosonic operators are non-standard and hence the Fokker-Planck equation is also unusual. Initial conditions, such as for initially uncorrelated states, are used to determine the initial distribution function. Transformations to new bosonic variables rotating at the cavity frequency enables the six coupled equations for the new c-number functions (also equivalent to the canonical Grassmann distribution function) to be solved analytically, based on an ansatz from a 1980 paper by Stenholm. It is then shown that the distribution function is the same as that determined from the well-known solution based on coupled equations for state vector amplitudes of atomic and n-photon product states. The treatment of the simple two fermion mode Jaynes-Cummings model is a useful test case for the future development of phase space Grassmann distribution functional methods for multi-mode fermionic applications in quantum-atom optics.Comment: 57 pages, 0 figures. Version

Discussing Quantum Aspects of Higher-Derivative 3D-Gravity in the First-Order Formalism

In this paper, we reassess the issue of deriving the propagators and identifying the spectrum of excitations associated to the vielbein and spin connection of (1+2)-D gravity in the presence of dynamical torsion, while working in the first-order formulation. A number of peculiarities is pointed out whenever the Chern-Simons term is taken into account along with a combination of bilinear terms in the torsion tensor. We present a procedure to derive the full set of propagators, based on an algebra of enlarged spin-type operators, and we discuss under which conditions the poles of the tree-level 2-point functions correspond to physical excitations that do not conflict with causality and unitarity

Dyson-Schwinger Equations: Density, Temperature and Continuum Strong QCD

Continuum strong QCD is the application of models and continuum quantum field theory to the study of phenomena in hadronic physics, which includes; e.g., the spectrum of QCD bound states and their interactions; and the transition to, and properties of, a quark gluon plasma. We provide a contemporary perspective, couched primarily in terms of the Dyson-Schwinger equations but also making comparisons with other approaches and models. Our discourse provides a practitioners' guide to features of the Dyson-Schwinger equations [such as confinement and dynamical chiral symmetry breaking] and canvasses phenomenological applications to light meson and baryon properties in cold, sparse QCD. These provide the foundation for an extension to hot, dense QCD, which is probed via the introduction of the intensive thermodynamic variables: chemical potential and temperature. We describe order parameters whose evolution signals deconfinement and chiral symmetry restoration, and chronicle their use in demarcating the quark gluon plasma phase boundary and characterising the plasma's properties. Hadron traits change in an equilibrated plasma. We exemplify this and discuss putative signals of the effects. Finally, since plasma formation is not an equilibrium process, we discuss recent developments in kinetic theory and its application to describing the evolution from a relativistic heavy ion collision to an equilibrated quark gluon plasma.Comment: 103 Pages, LaTeX, epsfig. To appear in Progress in Particle and Nuclear Physics, Vol. 4

Regression and the Maternal in the History of Psychoanalysis, 1900-1957

This paper examines the history of the concept of ‘regression’ as it was perceived by Sandor Ferenczi and some of his followers in the first half of the twentieth century. The first part provides a short history of the notion of ‘regression’ from the late nineteenth century to Ferenczi's work in the 1920s and 1930s. The second and third parts of the paper focus on two other thinkers on regression, who worked in Britain, under the influence of the Ferenczian paradigm – the interwar Scottish psychiatrist, Ian D. Suttie; and the British-Hungarian psychoanalyst, and Ferenczi's most important pupil, Michael Balint. Rather than a descriptive term which comes to designate a pathological mental stage, Ferenczi understood ‘regression’ as a much more literal phenomenon. For him, the mental desire to go backwards in time is a universal one, and a consequence of an inevitable traumatic separation from the mother in early childhood, which has some deep personal and cultural implications. The paper aims to show some close affinities between the preoccupation of some psychoanalysts with ‘regression’, and the growing interest in social and cultural aspects of ‘motherhood’ and ‘the maternal role’ in mid-twentieth-century British society

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