Remarks on the derivation of Gross-Pitaevskii equation with magnetic Laplacian

The effective dynamics for a Bose-Einstein condensate in the regime of high dilution and subject to an external magnetic field is governed by a magnetic Gross-Pitaevskii equation. We elucidate the steps needed to adapt to the magnetic case the proof of the derivation of the Gross-Pitaevskii equation within the "projection counting" scheme

Mean-field evolution of fermions with singular interaction

We consider a system of N fermions in the mean-field regime interacting though an inverse power law potential $V(x)=1/|x|^{\alpha}$, for $\alpha\in(0,1]$. We prove the convergence of a solution of the many-body Schr\"{o}dinger equation to a solution of the time-dependent Hartree-Fock equation in the sense of reduced density matrices. We stress the dependence on the singularity of the potential in the regularity of the initial data. The proof is an adaptation of [22], where the case $\alpha=1$ is treated.Comment: 16 page

Effective non-linear dynamics of binary condensates and open problems

We report on a recent result concerning the effective dynamics for a mixture of Bose-Einstein condensates, a class of systems much studied in physics and receiving a large amount of attention in the recent literature in mathematical physics; for such models, the effective dynamics is described by a coupled system of non-linear Sch\"odinger equations. After reviewing and commenting our proof in the mean field regime from a previous paper, we collect the main details needed to obtain the rigorous derivation of the effective dynamics in the Gross-Pitaevskii scaling limit.Comment: Corrected typos, updated reference

Cigarette smoke extract induced exosome release is mediated by depletion of exofacial thiols and can be inhibited by thiol-antioxidants

Introduction: Airway epithelial cells have been described to release extracellular vesicles (EVs) with pathological properties when exposed to cigarette smoke extract (CSE). As CSE causes oxidative stress, we investigated whether its oxidative components are responsible for inducing EV release and whether this could be prevented using the thiol antioxidants N-acetyl-L-cysteine (NAC) or glutathione (GSH). Methods: BEAS-2B cells were exposed for 24 h to CSE, H2O2, acrolein, 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB), bacitracin, rutin or the anti-protein disulfide isomerase (PDI) antibody clone RL90; with or without NAC or GSH. EVs in media were measured using CD63(+)CD81(+) bead-coupled flow cytometry or tunable resistive pulse sensing (TRPS). For characterization by Western Blotting, cryo-transmission electron microscopy and TRPS, EVs were isolated using ultracentrifugation. Glutathione disulfide and GSH in cells were assessed by a GSH reductase cycling assay, and exofacial thiols using Flow cytometry. Results: CSE augmented the release of the EV subtype exosomes, which could be prevented by scavenging thiol-reactive components using NAC or GSH. Among thiol-reactive CSE components, H2O2 had no effect on exosome release, whereas acrolein imitated the NAC-reversible exosome induction. The exosome induction by CSE and acrolein was paralleled by depletion of cell surface thiols. Membrane impermeable thiol blocking agents, but not specific inhibitors of the exofacially located thiol-dependent enzyme PDI, stimulated exosome release. Summary/conclusion: Thiol-reactive compounds like acrolein account for CSE-induced exosome release by reacting with cell surface thiols. As acrolein is produced endogenously during inflammation, it may influence exosome release not only in smokers, but also in ex-smokers with chronic obstructive pulmonary disease. NAC and GSH prevent acrolein-and CSE-induced exosome release, which may contribute to the clinical benefits of NAC treatment