C-Field Methods for Non-Equilibrium Bose Gases

We review c-field methods for simulating the non-equilibrium dynamics of degenerate Bose gases beyond the mean-field Gross-Pitaevskii approximation. We describe three separate approaches that utilise similar numerical methods, but have distinct regimes of validity. Systems at finite temperature can be treated with either the closed-system projected Gross-Pitaevskii equation (PGPE), or the open-system stochastic projected Gross-Pitaevskii equation (SPGPE). These are both applicable in quantum degenerate regimes in which thermal fluctuations are significant. At low or zero temperature, the truncated Wigner projected Gross-Pitaevskii equation (TWPGPE) allows for the simulation of systems in which spontaneous collision processes seeded by quantum fluctuations are important. We describe the regimes of validity of each of these methods, and discuss their relationships to one another, and to other simulation techniques for the dynamics of Bose gases. The utility of the SPGPE formalism in modelling non-equilibrium Bose gases is illustrated by its application to the dynamics of spontaneous vortex formation in the growth of a Bose-Einstein condensate.Comment: 7 pages, 1 figure. Unedited version of chapter to appear in Quantum Gases: Finite Temperature and Non-Equilibrium Dynamics (Vol. 1 Cold Atoms Series). N.P. Proukakis, S.A. Gardiner, M.J. Davis and M.H. Szymanska, eds. Imperial College Press, London (in press). See http://www.icpress.co.uk/physics/p817.html v2: Added arXiv cross-reference

Mean field effects on the scattered atoms in condensate collisions

We consider the collision of two Bose Einstein condensates at supersonic velocities and focus on the halo of scattered atoms. This halo is the most important feature for experiments and is also an excellent testing ground for various theoretical approaches. In particular we find that the typical reduced Bogoliubov description, commonly used, is often not accurate in the region of parameters where experiments are performed. Surprisingly, besides the halo pair creation terms, one should take into account the evolving mean field of the remaining condensate and on-condensate pair creation. We present examples where the difference is clearly seen, and where the reduced description still holds.Comment: 6 pages, 4 figure

Platelet Function in Paroxysmal Nocturnal Haemoglobinuria

Paroxysmal nocturnal haemoglobinuria (PNH) is a rare acquired clonal haematopoietic stem cell disorder characterised by haemolytic anaemia, thrombosis and bone marrow failure. Thrombosis is considered a major cause for high morbidity and mortality in PNH patients (Hillmen P et al N Eng J Med 1995). However, the underlying mechanisms of thrombosis in PNH are still poorly understood. Various factors including defective interactions between the complement system, platelets and coagulation systems have been proposed (Peacock-Young B et al Haematologica 2017). Platelet function and clot formation in this disorder have not been comprehensively evaluated. Here we describe standard and novel techniques to evaluate platelet function in blood from PNH patients, to elucidate the underlying pro-thrombotic mechanisms.MethodsWhole blood was collected from five PNH patients and compared to same-day healthy donor (HD) controls. The samples were collected at trough for those patients who were on eculizumab (Complement C5 inhibitor used in the treatment of PNH). Surface levels of platelet adhesion proteins and activation markers P-selectin and phosphatidylserine (PS) were assessed using flow cytometry. Plasma soluble GPVI (a platelet-specific activation marker) and cytokine levels were measured by ELISA. Clot formation was assessed by viscoelastic testing (ROTEM). Adhesion of platelets to collagen under flow in a whole blood assay was evaluated by Digital Holographic Microscopy (DHM) and thrombus height, surface area and volume quantified using custom-built MatLab-based software.ResultsClinical characteristics of PNH patients were highly variable: two patients had history of thrombosis, three patients were on eculizumab, four patients were thrombocytopenic (\\<150x109/L) and three were haemolysing. Platelet surface levels of adhesion/signalling receptor proteins including glycoproteins (GP) Iba, GPVI, aIIbb3, and ADAM10 (membrane expressed enzyme responsible for shedding GPVI from the surface) were all at lower ends of HD ranges. P-selectin and PS levels under resting and activated conditions and plasma soluble GPVI levels were comparable to same day HD. There were no differences between HD and PNH groups for levels of interleukin (IL) -6, IL-1β, tumour necrosis factor α, IL-17A, interferon γ or monocyte chemoattractant protein-1 (MCP-1). ROTEM analysis revealed slower formation of smaller clots in PNH patients, which correlated with their platelet count. Peak thrombus height and volume analysed by DHM were not different from data obtained with HD blood at both venous and arterial shear rates. However, both parameters were increased in PNH samples at arterial shearrate, when adjusted for platelet count (p\\<0.01).ConclusionAnalysis of these PNH patients with highly variable clinical characteristics did not identify a unifying platelet lesion. DHM could detect and quantify parameters of small thrombi in real time, in PNH patient samples and these data were consistent with enhanced thrombogenic potential in PNH patients. Mechanisms beyond platelet activation that contribute to increased thrombosis in these patients and the impact of eculizumab therapy on thrombotic propensity need to be explored further.D'Rozario:Alexion: Honoraria, Membership on an entity's Board of Directors or advisory committees