Multi-site Integrated Optical Addressing of Trapped Ions

One of the most effective ways to advance the performance of quantum computers and quantum sensors is to increase the number of qubits or quantum resources used by the system. A major technical challenge that must be solved to realize this goal for trapped-ion systems is scaling the delivery of optical signals to many individual ions. In this paper we demonstrate an approach employing waveguides and multi-mode interferometer splitters to optically address multiple $^{171}\textrm{Yb}^+$ ions in a surface trap by delivering all wavelengths required for full qubit control. Measurements of hyperfine spectroscopy and Rabi flopping were performed on the E2 clock transition, using integrated waveguides for delivering the light needed for Doppler cooling, state preparation, coherent operations, and detection. We describe the use of splitters to address multiple ions using a single optical input per wavelength and use them to demonstrate simultaneous Rabi flopping on two different transitions occurring at distinct trap sites. This work represents an important step towards the realization of scalable integrated photonics for atomic clocks and trapped-ion quantum information systems.Comment: 7 pages, 4 figures (+2 supplementary figures

A model for improving microbial biofuel production using a synthetic feedback loop

Cells use feedback to implement a diverse range of regulatory functions. Building synthetic feedback control systems may yield insight into the roles that feedback can play in regulation since it can be introduced independently of native regulation, and alternative control architectures can be compared. We propose a model for microbial biofuel production where a synthetic control system is used to increase cell viability and biofuel yields. Although microbes can be engineered to produce biofuels, the fuels are often toxic to cell growth, creating a negative feedback loop that limits biofuel production. These toxic effects may be mitigated by expressing efflux pumps that export biofuel from the cell. We developed a model for cell growth and biofuel production and used it to compare several genetic control strategies for their ability to improve biofuel yields. We show that controlling efflux pump expression directly with a biofuel-responsive promoter is a straightforward way of improving biofuel production. In addition, a feed forward loop controller is shown to be versatile at dealing with uncertainty in biofuel production rates

<it>Ureaplasma parvum </it>infection alters filamin a dynamics in host cells

<p>Abstract</p> <p>Background</p> <p><it>Ureaplasmas </it>are among the most common bacteria isolated from the human urogenital tract. <it>Ureaplasmas </it>can produce asymptomatic infections or disease characterized by an exaggerated inflammatory response. Most investigations have focused on elucidating the pathogenic potential of <it>Ureaplasma </it>species, but little attention has been paid to understanding the mechanisms by which these organisms are capable of establishing asymptomatic infection.</p> <p>Methods</p> <p>We employed differential proteome profiling of bladder tissues from rats experimentally infected with <it>U. parvum </it>in order to identify host cell processes perturbed by colonization with the microbe. Tissues were grouped into four categories: sham inoculated controls, animals that spontaneously cleared infection, asymptomatic urinary tract infection (UTI), and complicated UTI. One protein that was perturbed by infection (filamin A) was used to further elucidate the mechanism of <it>U. parvum</it>-induced disruption in human benign prostate cells (BPH-1). BPH-1 cells were evaluated by confocal microscopy, immunoblotting and ELISA.</p> <p>Results</p> <p>Bladder tissue from animals actively colonized with <it>U. parvum </it>displayed significant alterations in actin binding proteins (profilin 1, vinculin, α actinin, and filamin A) that regulate both actin polymerization and cell cytoskeletal function pertaining to focal adhesion formation and signal transduction (Fisher's exact test, P < 0.004; ANOVA, P < 0.02). This phenomenon was independent of clinical profile (asymptomatic vs. complicated UTI). We selected filamin A as a target for additional studies. In the BPH-1 model, we confirmed that <it>U. parvum </it>perturbed the regulation of filamin A. Specifically, infected BPH-1 cells exhibited a significant increase in filamin A phosphorylated at serine²¹⁵²(P ≤ 0.01), which correlated with impaired proteolysis of the protein and its normal intracellular distribution.</p> <p>Conclusion</p> <p>Filamin A dynamics were perturbed in both models of infection. Phosphorylation of filamin A occurs in response to various cell signaling cascades that regulate cell motility, differentiation, apoptosis and inflammation. Thus, this phenomenon may be a useful molecular marker for identifying the specific host cell pathways that are perturbed during <it>U. parvum </it>infection.</p