Microwave quantum optics and electron transport through a metallic dot strongly coupled to a transmission line cavity

We investigate theoretically the properties of the photon state and the electronic transport in a system consisting of a metallic quantum dot strongly coupled to a superconducting microwave transmission line cavity. Within the framework of circuit quantum electrodynamics we derive a Hamiltonian for arbitrary strong capacitive coupling between the dot and the cavity. The dynamics of the system is described by a quantum master equation, accounting for the electronic transport as well as the coherent, non-equilibrium properties of the photon state. The photon state is investigated, focusing on, for a single active mode, signatures of microwave polaron formation and the effects of a non-equilibrium photon distribution. For two active photon modes, intra mode conversion and polaron coherences are investigated. For the electronic transport, electrical current and noise through the dot and the influence of the photon state on the transport properties are at the focus. We identify clear transport signatures due to the non-equilibrium photon population, in particular the emergence of superpoissonian shot-noise at ultrastrong dot-cavity couplings.Comment: 19 pages, 10 figure

Release of neutrophil proteinase 4(3) and leukocyte elastase during phagocytosis and their interaction with proteinase inhibitors

Neutrophil proteinase 4 (NP4) is a major neutral proteinase of the human polymorphonuclear (PMN) leukocyte, which is present in amounts similar to leukocyte elastase. NP4(3) is a potent, non-specific proteinase, which may degrade structural and soluble proteins in the tissues and body fluids, and it has been implicated as an important pathogenetic factor in lung emphysema. We have studied the release of elastase and NP4(3) in an in vitro model of phagocytosis, α1-pproteinase inhibitor (α1-PI) is the major plasma inhibitor of both leukocyte elastase and NP4(3), but α1-PI bound leukocyte elastase more readily than NP4(3). The basic conditions were designed so that some proteolytic activity was present in the medium. Addition of increasing amounts of Secretory leukocyte protease inhibitor (SLPI) to the incubation mixtures resulted in binding of leukocyte elastase to this inhibitor and extinction of free proteolytic activity against both natural and synthetic substrates. The progressive binding of leukocyte elastase to SLPI instead of α1-PI was paralleled by an increasing binding of NP4(3) to α1-PI. SLPI is a potent inhibitor of leukocyte elastase and cathepsin G, and although it lacks inhibitory effect on NP4(3), it may obviously indirectly aid in the binding and inhibition of NP4(3) to α1-PI, by taking care of at least part of the leukocyte elastase. As a specific NP4(3)-inhibitor is not readily available for therapeutic use, this effect may prove useful under in vivo conditions and enhance the protective effect of administered recombinant human SLPI

Studies of the release and turnover of a human neutrophil lipocalin

A 24-kDa protein was purified from human neutrophil extracts and shown to be the newly discovered neutrophil gelatinase-associated lipocalin (NGAL), based on structural and immunochemical data. A specific enzyme-linked immunosorbent assay (ELISA) was developed for the determination of NGAL in human plasma and tissue fluids. Normal human plasma contains 72 μg 1-1 of NGAL (range 40-109 μg 1-1) in two main forms, monomer and dimer. 35S-methionine metabolic studies of human neutrophils showed that granulocyte macrophagecolony-stimulating factor (GMCSF) stimulated significant synthesis and secretion of NGAL in a dose- and time-dependent fashion. NGAL was rapidly released as monomer and dimer on incubation of heparinized whole blood with opsonized yeast, reaching a plateau corresponding to about 35% of total cell content after 30 min. Following intravenous injection of 125-iodine labelled NGAL there was a more rapid initial clearance of the monomeric than of the dimeric form; t1/2 10 min vs. 20 min. During the second phase the two forms cleared at similar rates. Severe acute peritonitis was accompanied by a 10-fold increase in NGAL plasma levels and the NGAL level in peritoneal exudates, which reached about 40 mg 1-1. There was a good linear correlation between the concentrations of NGAL, leucocyte elastase and NP4 (neutrophil proteinase 4 = P3)