Quantum Kinetic Evolution of Marginal Observables

We develop a rigorous formalism for the description of the evolution of observables of quantum systems of particles in the mean-field scaling limit. The corresponding asymptotics of a solution of the initial-value problem of the dual quantum BBGKY hierarchy is constructed. Moreover, links of the evolution of marginal observables and the evolution of quantum states described in terms of a one-particle marginal density operator are established. Such approach gives the alternative description of the kinetic evolution of quantum many-particle systems to generally accepted approach on basis of kinetic equations.Comment: 18 page

Towards Rigorous Derivation of Quantum Kinetic Equations

We develop a rigorous formalism for the description of the evolution of states of quantum many-particle systems in terms of a one-particle density operator. For initial states which are specified in terms of a one-particle density operator the equivalence of the description of the evolution of quantum many-particle states by the Cauchy problem of the quantum BBGKY hierarchy and by the Cauchy problem of the generalized quantum kinetic equation together with a sequence of explicitly defined functionals of a solution of stated kinetic equation is established in the space of trace class operators. The links of the specific quantum kinetic equations with the generalized quantum kinetic equation are discussed.Comment: 25 page

The von Neumann Hierarchy for Correlation Operators of Quantum Many-Particle Systems

The Cauchy problem for the von Neumann hierarchy of nonlinear equations is investigated. One describes the evolution of all possible states of quantum many-particle systems by the correlation operators. A solution of such nonlinear equations is constructed in the form of an expansion over particle clusters whose evolution is described by the corresponding order cumulant (semi-invariant) of evolution operators for the von Neumann equations. For the initial data from the space of sequences of trace class operators the existence of a strong and a weak solution of the Cauchy problem is proved. We discuss the relationships of this solution both with the $s$-particle statistical operators, which are solutions of the BBGKY hierarchy, and with the $s$-particle correlation operators of quantum systems.Comment: 26 page

Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation

The mammalian diffuse stellate cell system comprises retinoid-storing cells capable of remarkable transformations from a quiescent to an activated myofibroblast-like phenotype. Activated pancreatic stellate cells (PSCs) attract attention owing to the pivotal role they play in development of tissue fibrosis in chronic pancreatitis and pancreatic cancer. However, little is known about the actual role of PSCs in the normal pancreas. These enigmatic cells have recently been shown to respond to physiological stimuli in a manner that is markedly different from their neighbouring pancreatic acinar cells (PACs). Here, we demonstrate the capacity of PSCs to generate nitric oxide (NO), a free radical messenger mediating, for example, inflammation and vasodilatation. We show that production of cytosolic NO in PSCs is unambiguously related to cytosolic Ca2+ signals. Only stimuli that evoke Ca2+ signals in the PSCs elicit consequent NO generation. We provide fresh evidence for the striking difference between signalling pathways in PSCs and adjacent PACs, because PSCs, in contrast to PACs, generate substantial Ca2+-mediated and NOS-dependent NO signals. We also show that inhibition of NO generation protects both PSCs and PACs from necrosis. Our results highlight the interplay between Ca2+ and NO signalling pathways in cell–cell communication, and also identify a potential therapeutic target for anti-inflammatory therapies

Bile acids induce necrosis in pancreatic stellate cells dependent on calcium entry and sodium-driven bile uptake

Acute biliary pancreatitis, caused by bile reflux into the pancreas, is a serious condition characterised by premature activation of digestive enzymes within acinar cells, followed by necrosis and inflammation. Bile acids are known to induce pathological Ca2+ signals and necrosis in acinar cells. However, bile acid-elicited signalling events in stellate cells remain unexplored. This is the first study to demonstrate the pathophysiological effects of bile acids on stellate cells in two experimental models: ex vivo (mouse pancreatic lobules) and in vitro (human cells). Sodium cholate and taurocholate induced cytosolic Ca2+ elevations in stellate cells, larger than those elicited simultaneously in the neighbouring acinar cells. In contrast, taurolithocholic acid 3-sulfate (TLC-S), known to induce Ca2+ oscillations in acinar cells, had only minor effects on stellate cells in lobules. The dependence of the Ca2+ signals on extracellular Na+ and the presence of sodium-taurocholate cotransporting polypeptide (NTCP) indicate a Na+-dependent bile acid uptake mechanism in stellate cells. Bile acid treatment caused necrosis predominantly in stellate cells, which was abolished by removal of extracellular Ca2+ and significantly reduced in the absence of Na+, showing that bile-dependent cell death was a downstream event of Ca2+ signals. Finally, combined application of TLC-S and the inflammatory mediator bradykinin caused more extensive necrosis in both stellate and acinar cells than TLC-S alone. Our findings shed new light on the mechanism by which bile acids promote pancreatic pathology. This involves not only signalling in acinar cells but also in stellate cells

Bis(dihydrogen norfloxacinium) tri-μ2-chlorido-bis­[trichloridobismuthate(III)] chloride dihydrate

The title compound, {systematic name: (3-carb­oxy-1-ethyl-6-fluoro-7-piperazin-4-ium-1-yl-1H-quinolin-4-yl­idene)oxonium tri-μ2-chlorido-bis­[trichloridobismuthate(III)] chloride dihydrate], (C16H20FN3O3)2[Bi2Cl9]Cl·2H2O, is composed of [Bi2Cl9]3− anions lying on crystallographic twofold rotation axes, Cl− anions also on twofold axes, C16H20FN3O3 2+ cations, and water mol­ecules. The BiIII coordination polyhedron is a distorted octa­hedron and two such octa­hedra share a triangular face to form the complex anion. There are three short terminal Bi—Cl bonds [2.5471 (6)–2.5781(5 Å] and three longer bridging bonds [2.8599 (5)–2.9984 (6) Å] in each octa­hedron. Anions, cations and water mol­ecules are linked by hydrogen bonds to form a three-dimensional network. There are also π–π stacking inter­actions between quinoline ring systems, with an inter­planar distance of 3.27 (1) Å