Efficient production of polar molecular Bose-Einstein condensates via an all-optical R-type atom-molecule adiabatic passage

We propose a scheme of "$R$-type" photoassociative adiabatic passage (PAP) to create polar molecular condensates from two different species of ultracold atoms. Due to the presence of a quasi-coherent population trapping state in the scheme, it is possible to associate atoms into molecules with a \textit{low-power} photoassociation (PA) laser. One remarkable advantage of our scheme is that a tunable atom-molecule coupling strength can be achieved by using a time-dependent PA field, which exhibits larger flexibility than using a tunable magnetic field. In addition, our results show that the PA intensity required in the "$R$-type" PAP could be greatly reduced compared to that in a conventional "$\Lambda$-type" one.Comment: 17 pages, 5 figures, to appear in New Journal of Physic

A domain of spacetime intervals in general relativity

Beginning from only a countable dense set of events and the causality relation, it is possible to reconstruct a globally hyperbolic spacetime in a purely order theoretic manner. The ultimate reason for this is that globally hyperbolic spacetimes belong to a category that is equivalent to a special category of domains called interval domains.Comment: 25 page

Dynamic changes in macrophage populations and resulting alterations in Prostaglandin E2 sensitivity in mice with diet-induced MASH

Abstract Background The transition from metabolic dysfunction-associated steatotic liver disease (MASLD) to steatohepatitis (MASH) is characterized by a chronic low-grade inflammation, involving activation of resident macrophages (Kupffer cells; KC) and recruitment of infiltrating macrophages. Macrophages produce cytokines and, after induction of Cyclooxygenase 2 (COX-2), the key enzyme of prostanoid synthesis, prostaglandin E2 (PGE2). PGE2 modulates cytokine production in an autocrine and paracrine manner, therefore playing a pivotal role in regulating inflammatory processes. Changes in the hepatic macrophage pool during MASLD progression to MASH could influence PGE2- and cytokine-mediated signaling processes. The aim of this study was to characterize these changes in mice with diet-induced MASH and further elucidate the role of COX-2-dependently formed PGE2 on the inflammatory response in different macrophage populations of mice with a macrophage-specific COX-2-deletion. Methods Male, 6-7-week-old wildtype mice were fed either a Standard or high-fat, high-cholesterol MASH-inducing diet for 4, 12 and 20 weeks. Liver macrophages were isolated and analyzed by flow cytometry. For in vitro experiments primary KC, peritoneal macrophages (PM) and Bone-marrow-derived macrophages (BMDM) were isolated from macrophage-specific COX-2-deficient and wildtype mice and treated with lipopolysaccharide (LPS) and/or PGE2. Results During MASH-development, the proportion of KC (Clec4F+Tim4+) decreased, while the proportion of monocyte-derived macrophages (Clec4F−Tim4−) and monocyte-derived cells exhibiting a phenotype similar to KC (Clec4F+Tim4−) significantly increased over time. In vitro experiments showed that exogenous PGE2 completely abrogated the LPS-induced mRNA expression and secretion of tumor necrosis factor-alpha (TNF-α) in primary KC, PM and BMDM from wildtype mice. PM and BMDM, as in vitro models for infiltrating macrophages, were more sensitive to PGE2 compared to KC. Deletion of COX-2 in all macrophage populations led to an impaired PGE2-dependent feedback inhibition of TNF-α production. LPSinduced TNF-α mRNA expression was higher compared to the respective wildtype macrophage population. Conclusion The current study, using a murine MASH model, indicates that PGE2 may have a protective, anti-inflammatory effect, especially by inhibiting the expression of pro-inflammatory cytokines such as TNFα in infiltrating monocyte-derived macrophages. An inhibition of endogenous PGE2 synthesis in macrophages by pharmacological inhibition of COX-2 could potentially increase inflammation and promote the progression of MASH