Single-Shot Measurements of Phonon Number States Using the Autler-Townes Effect.

We present a single-shot method to measure motional states in the number basis. The technique can be applied to systems with at least three nondegenerate energy levels which can be coupled to a linear quantum harmonic oscillator. The method relies on probing an Autler-Townes splitting that arises when a phonon-number changing transition is strongly coupled.

Submicrosecond entangling gate between trapped ions via Rydberg interaction.

Generating quantum entanglement in large systems on timescales much shorter than the coherence time is key to powerful quantum simulation and computation. Trapped ions are among the most accurately controlled and best isolated quantum systems with low-error entanglement gates operated within tens of microseconds using the vibrational motion of few-ion crystals. To exceed the level of complexity tractable by classical computers the main challenge is to realize fast entanglement operations in crystals made up of many ions (large ion crystals).

Tracking the Dynamics of an Ideal Quantum Measurement.

The existence of ideal quantum measurements is one of the fundamental predictions of quantum mechanics. In theory, an ideal measurement projects a quantum state onto the eigenbasis of the measurement observable, while preserving coherences between eigenstates that have the same eigenvalue. The question arises whether there are processes in nature that correspond to such ideal quantum measurements and how such processes are dynamically implemented in nature.

PA5oct Jumbo Phage Impacts Planktonic and Biofilm Population and Reduces Its Host Virulence.

The emergence of phage-resistant mutants is a key aspect of lytic phages-bacteria interaction and the main driver for the co-evolution between both organisms. Here, we analyze the impact of PA5oct jumbo phage treatment on planktonic/cell line associated and sessile population. Besides its broad-spectrum activity and efficient bacteria reduction in both airway surface liquid (ASL) model, and biofilm matrix degradation, PA5oct appears to persist in most of phage-resistant clones.

Highly Polarizable Rydberg Ion in a Paul Trap.

Usually the influence of the quadratic Stark effect on an ion's trapping potential is minuscule and only needs to be considered in atomic clock experiments. In this work we excite a trapped ion to a Rydberg state with polarizability ∼8 orders of magnitude higher than a low-lying electronic state; we find that the highly polarizable ion experiences a vastly different trapping potential owing to the Stark effect. We observe changes in trap stiffness, equilibrium position, and minimum potential, which can be tuned using the trapping electric fields.

Effective nebulization of interferon-γ using a novel vibrating mesh.

Background: Interferon gamma (IFN-γ) is a clinically relevant immunomodulatory cytokine that has demonstrated significant potential in the treatment and management of respiratory diseases such as tuberculosis and pulmonary fibrosis. As with all large biomolecules, clinical translation is dependent on effective delivery to the disease site and delivery of IFN-γ as an aerosol offers a logical means of drug targeting. Effective localization is often hampered by instability and a lack of safe and efficient delivery systems.

Coherent Control of a Single Trapped Rydberg Ion.

Trapped Rydberg ions are a promising novel approach to quantum computing and simulations. They are envisaged to combine the exquisite control of trapped ion qubits with the fast two-qubit Rydberg gates already demonstrated in neutral atom experiments. Coherent Rydberg excitation is a key requirement for these gates.

Resolvin D1 regulates epithelial ion transport and inflammation in cystic fibrosis airways.

Background: Cystic Fibrosis (CF) lung disease is characterised by dysregulated ion transport that promotes chronic bacterial infection and inflammation. The impact of the specialised pro-resolution mediator resolvin D1 (RvD1) on airway surface liquid (ASL) dynamics and innate defence had not yet been investigated in CF airways.

Methods: Ex vivo studies were performed on primary cultures of alveolar macrophages and bronchial epithelial cells from children with CF and in human bronchial epithelial cell lines; in vivo studies were performed in homozygous F508del-CFTR mice treated with vehicle control or RvD1 (1-100nM).

A proposed integrated approach for the preclinical evaluation of phage therapy in Pseudomonas infections.

Bacteriophage therapy is currently resurging as a potential complement/alternative to antibiotic treatment. However, preclinical evaluation lacks streamlined approaches. We here focus on preclinical approaches which have been implemented to assess bacteriophage efficacy against Pseudomonas biofilms and infections.

Lipoxin A4 prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells by Pseudomonas aeruginosa.

The specialized proresolution lipid mediator lipoxin A4 (LXA4) is abnormally produced in cystic fibrosis (CF) airways. LXA4 increases the CF airway surface liquid height and stimulates airway epithelial repair and tight junction formation. We report here a protective effect of LXA4 (1 nM) against tight junction disruption caused by Pseudomonas aeruginosa bacterial challenge together with a delaying action against bacterial invasion in CF airway epithelial cells from patients with CF and immortalized cell lines.

miR-17 overexpression in cystic fibrosis airway epithelial cells decreases interleukin-8 production.

Interleukin (IL)-8 levels are higher than normal in cystic fibrosis (CF) airways, causing neutrophil infiltration and non-resolving inflammation. Overexpression of microRNAs that target IL-8 expression in airway epithelial cells may represent a therapeutic strategy for cystic fibrosis. IL-8 protein and mRNA were measured in cystic fibrosis and non-cystic fibrosis bronchoalveolar lavage fluid and bronchial brushings (n=20 per group).

Physiological impact of abnormal lipoxin A₄ production on cystic fibrosis airway epithelium and therapeutic potential.

Lipoxin A4 has been described as a major signal for the resolution of inflammation and is abnormally produced in the lungs of patients with cystic fibrosis (CF). In CF, the loss of chloride transport caused by the mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel gene results in dehydration, mucus plugging, and reduction of the airway surface liquid layer (ASL) height which favour chronic lung infection and neutrophil based inflammation leading to progressive lung destruction and early death of people with CF. This review highlights the unique ability of LXA4 to restore airway surface hydration, to stimulate airway epithelial repair, and to antagonise the proinflammatory program of the CF airway, circumventing some of the most difficult aspects of CF pathophysiology.

Physiological levels of lipoxin A4 inhibit ENaC and restore airway surface liquid height in cystic fibrosis bronchial epithelium.

In cystic fibrosis (CF), the airway surface liquid (ASL) is depleted. We previously demonstrated that lipoxin A4 (LXA4) can modulate ASL height (ASLh) through actions on Cl(-) transport. Here, we report novel effects of lipoxin on the epithelial Na(+) channel ENaC in this response.

Activation of P2RY11 and ATP release by lipoxin A4 restores the airway surface liquid layer and epithelial repair in cystic fibrosis.

In cystic fibrosis (CF), the airway surface liquid (ASL) height is reduced as a result of impaired ion transport, which favors bacterial colonization and inflammation of the airway and leads to progressive lung destruction. Lipoxin (LX)A4, which promotes resolution of inflammation, is inadequately produced in the airways of patients with CF. We previously demonstrated that LXA4 stimulates an ASL height increase and epithelial repair.

The role of Lipoxin A4 in Cystic Fibrosis Lung Disease.

In Cystic Fibrosis (CF), mutations of the CFTR gene result in defective Cl(-) secretion and Na(+) hyperabsorption by epithelia which leads to airway lumen dehydration and mucus plugging and favours chronic bacterial colonization, persistent inflammation and progressive lung destruction. Beyond this general description, the pathogenesis of CF lung disease remains obscure due to an incomplete understanding of normal innate airway defense. This mini-review aims to highlight the role of the pro-resolution lipid mediator, Lipoxin A4, which is inadequately produced in CF, on several aspects of innate immunity that are altered in CF airway disease.

Lipoxin A4 stimulates calcium-activated chloride currents and increases airway surface liquid height in normal and cystic fibrosis airway epithelia.

Cystic Fibrosis (CF) is a genetic disease characterised by a deficit in epithelial Cl(-) secretion which in the lung leads to airway dehydration and a reduced Airway Surface Liquid (ASL) height. The endogenous lipoxin LXA(4) is a member of the newly identified eicosanoids playing a key role in ending the inflammatory process. Levels of LXA(4) are reported to be decreased in the airways of patients with CF.

Toward exceeding the Shockley-Queisser limit: photoinduced interfacial charge transfer processes that store energy in excess of the equilibrated excited state.

Nanocrystalline (anatase), mesoporous TiO2 thin films were functionalized with [Ru(bpy)2(deebq)](PF6)2, [Ru(bq)2(deeb)](PF6)2, [Ru(deebq)2(bpy)](PF6)2, [Ru(bpy)(deebq)(NCS)2], or [Os(bpy)2(deebq)](PF6)2, where bpy is 2,2'-bipyridine, bq is 2,2'-biquinoline, and deeb and deebq are 4,4'-diethylester derivatives. These compounds bind to the nanocrystalline TiO2 films in their carboxylate forms with limiting surface coverages of 8 (+/- 2) x 10(-8) mol/cm2. Electrochemical measurements show that the first reduction of these compounds (-0.

Intermolecular energy transfer across nanocrystalline semiconductor surfaces.

The yields and dynamics for energy transfer from the metal-to-ligand charge-transfer excited states of Ru(deeb)(bpy)(2)(PF(6))(2), Ru(2+), and Os(deeb)(bpy)(2)(PF(6))(2), Os(2+), where deeb is 4,4'-(CH(3)CH(2)CO(2))(2)-2,2'-bipyridine, anchored to mesoporous nanocrystalline (anatase) TiO(2) thin films were quantified. Lateral energy transfer from Ru(2+)* to Os(2+) was observed, and the yields were measured as a function of the relative surface coverage and the external solvent environment (CH(3)CN, THF, CCl(4), and hexanes). Excited-state decay of Ru(2+)*/TiO(2) was well described by a parallel first- and second-order kinetic model, whereas Os(2+)*/TiO(2) decayed with first-order kinetics within experimental error.